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Current Issue
31 March 2024, Volume 21 Issue 2
Previous Issue
Comparison of Protein Characteristics of Human WASH468 and WASH465
#br#
ZHENG Aixue, ZHANG Luping, TANG Tuo, LI Ping, HONG Xian, DENG Zhihui, WANG Tao
2024, 21(2): 93-99. doi:
10.3870/j.issn.1672-8009.2024.02.001
Abstract
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Objective
To investigate the differences between two well recognized WiskottAldrich syndrome protein and SCAR homolog ( WASH) with different sequences.
Methods
Immunofluorescence, immunoprecipitation, and laser micro-irradiation were used to analyze the differences between WASH468 and WASH465 in localization patterns, the interaction with FAM21 or Ku proteins, the recruitment to DNA damage sites and the protein stabilities. To analyze the universality and conservation of the two types of WASH sequences, the WASH protein sequences in various organisms were compared, and the WASH coding sequences in various cell types commonly used forbiological and medical research were detected.
Results
Both WASH exhibited a similar way in localizing to endosome. WASH468 exhibited a stronger interaction with FAM21, and was more stable than WASH465. WASH465 exhibited a stronger interaction with Ku protein, and the recruitment of
WASH465 to DNA damage sites was more robust than that of WASH468. The degree of similarity observed between the sequence of WASH468 in humans and the sequences of WASH in other organisms was significantly greater than that observed with WASH465. Moreover, the coding sequences of WASH in various cell types, which are commonly utilized in biological and medical research, exhibited concordance with the sequence of WASH468.
Conclusion
There are differences in the biological characteristics between WASH468 and WASH465, and WASH468 is significantly more universal and conserved than WASH465. Therefore, WASH468 is the conserved human WASH sequence.
Role of Circulating Eosinophils Mediated by Plasma SPARC in Gastric Cancer
:
A Multivariable Mendelian Randomization Study and Mediation Analysis
#br#
HAN Zhengxuan, YANG Chaogang, XIONG Hao, XIONG Bin,
2024, 21(2): 100-107. doi:
10.3870/j.issn.1672-8009.2024.02.002
Abstract
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Objective
East Asia exhibits one of the highest global incidence rates of gastriccancer. The intricate relationship between peripheral blood immune cell counts and the onset and progression of gastric cancer is often obscured by reverse causality and confounders. This study employs Mendelian randomization analysis to mitigate associated biases, aiming to elucidate the causalconnection between peripheral immune cell counts and gastric cancer.
Methods
Both univariateand multivariate Mendelian randomization methods were employed to explore the causal relationship
between diverse immune cell subtypes in peripheral blood and the risk of gastric cancer using data from Genome-wide association studies ( GWAS). Exposure factors included counts of white blood cells, granulocytes, neutrophils, eosinophils, basophils, lymphocytes, and monocytes. The primary approach for univariate Mendelian randomization analysis involved the inverse variance-weighted method. Afterwards, a two-step mediation analysis was conducted to investigate the potential roleof plasma proteins in this process.
Results
Mendelian randomization analysis revealed a causal relationship between lymphocytes (
OR
= 1. 094, 95 %
CI
: 1. 009-1. 185,
P
= 0. 029) and eosinophils (
OR
= 0. 881, 95 %
CI
: 0. 813-0. 955,
P
= 0. 002 ) and the incidence of gastric cancer. Sensitivity analysis corroborated the reliability of these results. Furthermore, the association between decreased eosinophil counts and a reduced risk of gastric cancer persisted in multivariate Mendelian randomization analysis (
OR
= 0. 807, 95 %
CI
: 0. 671-0. 970,
P
= 0. 023). Reverse causality was not significant. The secreted protein acidic and rich in cysteine (SPARC) is an extracellular matrix protein that involves in various cell-matrix interactions and cellular signaling pathways, playing a significant role in tumor development. The mediation analysis of 1 124 plasma proteins suggested that plasma SPARC might mediate the protective effect of eosinophils against gastric cancer(Beta = - 0. 030, 95 %
CI
: - 0. 072-0. 000,
P
= 0. 024).
Conclusion
Mendelian randomizationanalysis establishes eosinophil counts as an independent factor in diminishing the incidence of gastric cancer. Plasma SPARC acts as a mediator in this process, suggesting that circulating eosinophil count and plasma SPARC have the potential to become early clinical indicators and therapeutic targets for gastric cancer. The Mendelian randomization method effectively mitigates biases stemming from reverse causality and psychosocial factors. Nevertheless, additional research is imperative to validate its underlying biological mechanisms.
Effect of PKM2 Neddylation Modification on Right Ventricular Fibrosis in Pulmonary Hypertension Rats
#br#
GUO Wenyun, WANG Lixia, WANG Jinlin
2024, 21(2): 108-114. doi:
10.3870/j.issn.1672-8009.2024.02.003
Abstract
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Objective
Exploring the effect of PKM2 neddylation modification on myocardial fibrosis in pulmonary hypertension rats.
Methods
SD rats were randomly divided into 3 groups: control group, model group, and MLN4924 group. Pulmonary arteries were detected by HE staining, and right ventricular fibrosis was detected by Masson staining. Primary cardiac fibroblasts were isolated from rats and the expression of α-Smooth muscle actin (α-SMA) was measured by immunofluorescence assay. The si-NC, si-PKM2, and pcDNA3. 1-PKM2 were transfected into the primary cardiac fibroblasts and the expression levels of PKM2, fibrosis related proteins Collagen Ⅰ , Collagen Ⅲ , MMP2, and MMP9 were detected by Western blotting. Immunoprecipitation assay was used to detect the PKM2 neddylation modification. Real time fluorescence quantitative PCR method was used to detect the mRNA expression level of PKM2 in the rat heart tissues. The degradation of PKM2 protein was detected by Western blotting, and the half-life of PKM2 was determined.
Results
The HE staining results showed that the space between pulmonary arterioles (fibrous layer) and intima (inner transport protein) in the model group was significantly widened and the intermediate layer were
thickened. Masson staining showed that the collagen deposition was increased and the fibrosis was more severe in the model group when compared with those in the control group. The expression level of PKM2 protein in the model group was higher than that in the control group, while there was no significant difference in the mRNA expression level. PKM2 underwent neddylation modification in the right ventricular tissues of pulmonary hypertension rats. Knocking down Nedd8 in cardiac fibroblasts or inhibiting neddylation modification with MLN4924 could downregulate the expression levels of PKM2 and fibrosis related proteins Collagen Ⅰ , Collagen Ⅲ , MMP2, MMP9, etc. , promotingthe degradation of PKM2 protein [ (3. 03 ± 0. 23) - (11. 97 ± 0. 66) h,
t
= - 12. 82,
P
<0. 001] . However, the overexpression of Nedd8 could increase the expression level of PKM2 protein. The degree of right ventricular fibrosis and the expression level of α-SMA protein in theMLN4924 group were lower than those in the model group.
Conclusion
Neddylation modificationenhances the protein stability of PKM2, thereby promoting the process of right ventricular fibrosis inthe rat model of pulmonary arterial hypertension.
LncHAGLR Promotes Inflammatory Response and Apoptosis of Chondrocytes in Osteoarthritis Rats by Targeting miR-26a and Activation of NF-κB
#br#
MENG Xiaoyuan, Wuerkan Yeerken, WANG Zhigang, MA Le
2024, 21(2): 115-123. doi:
10.3870/j.issn.1672-8009.2024.02.004
Abstract
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To investigate the effect and potential mechanism of long non-codingRNA HAGLR on the inflammatory response and apoptosis of chondrocytes in rats with osteoarthritis.
Methods
StarBase and luciferase gene reporter assay were used to predict and verify the interaction between lncHAGLR and miR-26a. To investigate the regulatory role of lncHAGLR on miR-26a expression, C518 cells were divided into 4 groups: si-lncHAGLR group, si-NC group, miR-26ainhibitor group, and inhibitor-NC group. Furthermore, to study whether lncHAGLR regulates in
flammation and apoptosis in C518 cells by modulating miR-26a, C518 cells were divided into 5 groups: Control group, IL-1β group, IL-1β + si-NC group, IL-1β + si-lncHAGLR group, and IL-1β + si-lncHAGLR + miR-26a-inhibitor group. Real-time quantitative PCR ( qRT-PCR) was used to analyze the expression levels of lncHAGLR and miR-26a. The proliferation, cytotoxicity and apoptosis of C518 cells were detected by MTT, lactate dehydrogenase (LDH) Kit and flow cytometry (FCM). Western blotting assay was used to detect the protein expression levels of cleavedCASPASE3, NF-κB P65, and phosphorylated NF-κB P65 (P-NF-κB P65). The levels of releasedinflammatory factors (TNF-α and IL-6) were detected by ELISA.
Results
lncHAGLR directly targeted miR-26a. The expression level of lncHAGLR in the IL-1β group was significantly higher than that in the Control group, and the expression level of miR-26a was significantly lower than that inthe Control group (all
P
< 0. 05). In addition, cells in the IL-1β + si-lncHAGLR group had reducedIL-1β-induced chondrocyte inflammation, inhibited apoptosis, increased cell viabilities, decreased release of LDH, inhibited expression of cleaved-CASPASE3, and decreased secretions of TNF-αand IL-6 ( all
P
< 0. 05). Moreover, the expression level of P-NF-κB P65 was decreased (
P
<0. 05). Adding of miR-26a-inhibitor ( IL-1β + si-lncHAGLR + miR-26a-inhibitor group) reversedthe performances of cells in the IL-1β + si-lncHAGLR group (all
P
< 0. 05).
Conclusion
lncHAGLR promotes the inflammatory response and apoptosis of chondrocytes in osteoarthritis rats by inhibiting the activation of NF-κB through targeting miR-26a, suggesting that lncHAGLR may be avaluable therapeutic target for osteoarthritis treatment.
Correlation Analysis of Serum Asprosin Levels and Elderly Patients with Type 2 Diabetic Nephropathy
#br#
LIU Tian, FAN Jingjing, CHEN Mengnan, GUO Mengyuan, LU Hailong
2024, 21(2): 124-128. doi:
10.3870/j.issn.1672-8009.2024.02.005
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To analyze the correlation between serum Asprosin levels and elderlytype 2 diabetic nephropathy (DN) to provide clues for the search of new early indicators of DN inclinical practice.
Methods
A total of 183 patients with type 2 diabetes mellitus (T2DM) admittedto our hospital from August 2021 to March 2022 were included for this study. According to whether the patients have DN or not, the patients were divided into 2 groups: the T2DM group alone (85 cases) and the combined DN group (98 cases). Another 50 healthy patients were selected for the control group. The serum Asposin levels in each group was detected and the diagnostic efficacy of Asposin in early DN was analyzed.
Results
Asprosin levels were significantly higher in the T2DMgroup [ (1. 64 ± 0. 41) ng / mL] and the combined DN group [ (2. 45 ± 0. 52) ng / mL] whencompared with that in the control group [ (1. 15 ± 0. 23 ng / mL], and Asprosin level in the combined DN group was higher than that in the T2DM group (
P
< 0. 05). Asprosin level was positively correlated with the values of BUN, Cr, UA, HbA1c, FINS, HOMA-IR, UAER (
P
< 0. 05 ) . The level of Asprosin, HbA1c and UAR were risk factors affecting the occurrence of DN (
P
<0. 05). The area under the curve for the diagnosis of DN by Asprosin combined with UAER was0. 879 (95 %
CI
: 0. 813-0. 974,
P
< 0. 05), the diagnostic specificity was 84. 19 % , and thesensitivity was 94. 57 % .
Conclusion
Elderly DN patients exhibit higher expression of serum Asprosin levels, which may serve as an early diagnostic indicator for the presence of diabetic nephropathy in elderly type 2 diabetes patients.
Role of CCDC25 Mediated Neutrophil Extracellular Traps in Promoting Proliferation
,
Migration and Invasion of Osteosarcoma Cells
#br#
Muteli Maimaiti, XU Leilei, LI Wenqiang, YAN Feihua
2024, 21(2): 129-134. doi:
10.3870/j.issn.1672-8009.2024.02.006
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To investigate the role and underlying mechanisms of neutrophil extracellular traps ( NETs ) in the proliferation, migration, and invasion of osteosarcomacells.
Methods
A total of 20 osteosarcoma patients and 20 healthy subjects were enrolled. Levels ofPAD4 and H3cit in serum were measured by ELISA. Neutrophils were isolated from peripheral blood of both groups to compare NETs formation. Co-culturing experiments were conducted by incubating NETs with osteosarcoma cells (MG63), with the addition of DNA degrading enzyme DNaseⅠ . The groups included Control, NETs, and NETs + DNase Ⅰ groups. CCDC25 protein expression level was detected using Western blotting, cell proliferation was assessed using CCK-8 assay, and cell migration and invasion were evaluated using Transwell assay. MG63 cells were transfected with si-NC and si-CCDC25, then co-cultured with NETs, cells were then divided into 2 groups: si-NC and siCCDC25 groups. CCDC25 protein expression, cell proliferation, and invasion were assessed as described above.
Results
Compared to healthy subjects, osteosarcoma patients showed elevated levels of PAD4 and H3cit in serum (
P
< 0. 05 ), indicating enhanced NETs formation capaci
ty. Compared to the Control group, the NETs group exhibited elevated CCDC25 protein expressionlevel, increased cell proliferation and cell migration and invasion (
P
< 0. 05). The NETs + DNaseⅠ group showed reduced CCDC25 protein expression level, decreased cell proliferation, cell migration and invasion compared to the NETs group (
P
< 0. 05). The si-CCDC25 group, when compared to the si-NC group, demonstrated decreased CCDC25 protein expression level, cell proliferation, cell migration and invasion (P<0.05).
Conclusion
NETs activate osteosarcoma cell CCDC25 expression through released DNA, thereby promoting tumor cell proliferation, and cell migration and invasion.
Effect of Sufentanil on Cervical Cancer Cell Cycle and Apoptosis Through Long Non-coding RNA CCAT1
#br#
WEN Xu, PANG Xiaoyi, WEN Yan, WANG Rong, DU Qian, XIAO Song
2024, 21(2): 135-140. doi:
10.3870/j.issn.1672-8009.2024.02.007
Abstract
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To investigate the molecular mechanisms by which sufentanil affects cervical cancer (CC) cells.
Methods
Real-time quantitative PCR ( RT-qPCR) assay was used todetect the expression level of lncRNA CCAT1 in CC tissues and precancerous tissues, and in the cervical epithelial cells GH329 and CC cell lines (HeLa, CaSki, Siha and C4-1) . Subsequently, CC cells CaSki were randomly divided into 4 groups: blank group, sufentanil group, sufentanil + oe-NC group and sufentanil + CCAT1 group. RT-qPCR assay was then used to examine the expression level of lncRNA CCAT1 in each group. Cell Counting Kit-8 (CCK-8) assay was used to detect the cell proliferation ability. Flow cytometry was used to detect the changes of cell cycle and the cellapoptosis.
Results
lncRNA CCAT1 was highly expressed in CC tissues and the CC cell lines (HeLa, CaSki, Siha and C4-1) when compared with that in the precancerous tissues and that in theGH329 cells respectively (
P
< 0. 01) . The expression level of lncRNA CCAT1 in and the proliferation ability of CaSki cells were significantly decreased (
P
< 0. 01), while the proportion of cells in
the G
0
/ G
1
phase and the apoptosis rate were significantly increased (
P
<0. 01) in the sufentanil groupwhen compared with those in the blank group. The expression level of lncRNA CCAT1 and the proliferation ability of CaSki cells in the sufentanil + oe-CCAT1 group were significantly increased (
P
< 0. 01), while the proportion cells in the G
0
/ G
1
phase and cell apoptosis rate were significantly decreased (
P
<0. 01) when compared with those in the sufentanil + oe-NC group.
Conclusion
Sufentanil could blockthe CC cell cycle by decreasing lncRNA CCAT1 expression in CC cells, ultimately inhibiting the proliferative ability of CC cells and promoting cell apoptosis.
Sennoside B Inhibits the Proliferation
,
Apoptosis and Invasion of Retinoblastoma HXO-Rb44 Cells via Wnt / β-catenin Pathway
#br#
SUN Mengmeng, CUI Bokun, JIA Meng, RAN Liu, WANG Danrong, FENG Suting, ZHANG Hu, HAO Jianzhang
2024, 21(2): 141-145. doi:
10.3870/j.issn.1672-8009.2024.02.008
Abstract
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To investigate the effect of sennoside B on proliferation, apoptosis, invasion and Wnt / β-catenin signaling pathway of retinoblastoma HXO-Rb44 cells.
Methods
HXORB44 cells were treated with different doses (0, 5, 10 and 20 μmol / L) of sennoside B, and the cells were randomly divided into four groups: Control group, sennoside B 5 μmol / L group, sennoside B 10 μmol / L group and sennoside B 20 μmol / L group. Cell viability was detected by MTT assay. Colony formation assay was used to detect the colony formation rate. Cell apoptosis rate was detected by flow cytometry. Cell invasion were detected by Transwell assay. Cell pellet-forming experiment was used to detect the diameters and numbers of cell pellets. The protein expression levels of Cleaved Caspase-3, Caspase-3, MMP-2, MMP-9, SOX2, OCT4, CD44, Wnt1, β-cateninwere detected by Western blotting.
Results
The cell viabilities and colony formation rates in thesennoside B 10 and 20 μmol / L groups were significantly decreased when compared with those in theControl group (
P
< 0. 05), the cell apoptosis rates and cleaved Caspase-3 / Caspase-3 expression levels were significantly increased when compared with those in the Control group (
P
< 0. 05). Thenumbers of invaded cells and the protein expression levels of MMP-2 and MMP-9 were significantlydecreased in the sennoside B 10 and 20 μmol / L groups (
P
< 0. 05), the cell pellet diameters, thecell pellet numbers and the protein expression levels of SOX2, OCT4 and CD44 were significantly
decreased (
P
< 0. 05), and the protein expression levels of Wnt1 and β-catenin were significantlydecreased in the sennoside B 10 and 20 μmol / L groups when compared with those in the Controlgroup (
P
< 0. 05).
Conclusion
Sennoside B can induce apoptosis, inhibit the proliferation, invasion and stem-like characteristics of retinoblastoma HXO-Rb44 cells, and inhibit the activation of Wnt / β-catenin signaling pathway.
Resveratrol Inhibits Renal Fibrosis and Reduces Kidney Damage Caused by Unilateral Ureteral Obstruction
#br#
ZHAN Hongyi, SONG Yaling, HE Shaolin, ZHOU Yangyang
2024, 21(2): 146-153. doi:
10.3870/j.issn.1672-8009.2024.02.009
Abstract
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To investigate the effect of resveratrol on renal fibrosis and kidney damage induced by unilateral ureteral obstruction and its related mechanism.
Methods
Sprague-dawley( SD) rats and NRK-49F fibroblasts were used as experimental subjects for
in vivo
study and
in vitro
validation.
In vivo
, TIF rat model was establish by surgery to induce the unilateral ureteral obstruction in SD rats, and the rats were then randomly divided into 4 groups: sham operation + blankgroup, sham operation + resveratrol group, model + blank group and model + resveratrol group, 12rats in each group.
In vitro
: NRK-49F cells were treated with recombinant TGF-β1 (5 ng / mL) orresveratrol (10 and 100 μmol / L) and randomly divided into 4 groups: control group, TGF-β1 group, TGF-β1 + resveratrol low-dose group and TGF-β + resveratrol high-dose group. Masson’ s staining was used to detect total collagen deposition in the kidney. Immunohistochemical staining was used to detect the expression of E-cadherin, GFAP and Ki67 in the tissues. Immunofluorescence staining was used to detect the expression of Ki67 in cells. Western blotting was used to detect the expression level of Vimentin, N-cadherin, Racl, c-Myc, Bcl-2, Cyclin D1, α-SMA, type I collagen and type Ⅲ collagen, E-cadherin.
Results
Resveratrol could inhibit the excessive depositionof total collagen in kidneys of UUO rats, down-regulate α-SMA-positive myofibroblasts, reduce the
expression of vimentin, type I and type Ⅲ collagen, and inhibit the up-regulation of Rac1, GFAP and down-regulation of N-cadherin. Resveratrol could significantly reduce the ratio of Ki67-positive cells in UUO rats and inhibit the expression level of c-Myc, Bcl-2 and cyclin D1. Resveratrol inhibited the activation of proliferation-related pathway Wnt / β-catenin. The
in vitro
experimentsshowedthat resveratrol treatment could reduce the proliferation of fibroblasts and TECs, thereby inhibiting
TGF-β1-mediated phenotypic transformation and ECM accumulation.
Conclusion
Resveratrol in
hibits the activity of Wnt / β-catenin pathway and the accumulation of myofibroblasts, and reduces
renal tubulointerstitial fibrosis.
Expressions of miR-144-3p and Its Target Gene
PTEN
in Ovarian Granule Cells and Their Functions in Patients with Polycystic Ovary Syndrome
#br#
SU Jing, ZHANG Rongxue, ZHONG Jixiang, QIU Fenglong, JIA Yuanyuan, XUE Huiying
2024, 21(2): 154-160. doi:
10.3870/j.issn.1672-8009.2024.02.010
Abstract
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Objective
To investigate the expressions of miR-144-3p and its target gene
PTEN
in ovarian granule cells and their functions in patients with polycystic ovary syndrome.
Methods
Twenty patients with PCOS and 20 controls were recruited. Granulosa cells were collected in both groups and the expression level of miR-144-3p in cells was analyzed. The target genes of miR-144-3p were predicted by TargetScan database, and the binding relationship was verified by dual luciferase gene reporter assay. The human ovarian granulosa cells ( KGN) were resuscitated and transfected with miR-144-3p mimic / mimic NC, or miR-144-3p inhibitor / inhibitor NC, or si-PTEN / siRNANC, and were then accordingly divided into 6 groups: miR-144-3p mimic group, mimic NC group, miR-144-3p inhibitor group, inhibitor NC group, si-PTEN and siRNA-NC group. Cell apoptosis was detected by TUNEL assay. RT-PCR and Western blotting method were used to detect the
relative expression levels of miR-144-3p and PTEN.
Results
RT-PCR results showed that the expression level of miR-144-3p in the PCOS group was significantly lower than that in the control group(
P
< 0. 05). Flow cytometry results showed that the apoptosis rate of granulosa cells in the miR-144- 3p mimic group was significantly lower than that in the mimic-NC group (
P
< 0. 05), while the apoptosis rate of granulosa cells in the miR-144-3p inhibitor group was significantly higher than that inthe inhibitor-NC group (
P
< 0. 05).
PTEN
was predicted as the target gene of miR-144-3p by bioinformatics analysis, and the luciferase gene reporter experiments had confirmed that miR-144-3pcould specifically bind to the PTEN-3 ′ UTR and down-regulate the expression level of
PTEN
gene. RT-PCR assay results showed that the expression level of
PTEN
mRNA in the PCOS group was significantly higher than that in the control group (
P
< 0. 05), and was negatively correlated with the expression level of miR-144-3p (
r
= - 0. 91,
P
< 0. 001). The results of qRT-PCR and Westernblotting showed that the mRNA and protein expression levels of PTEN in the miR-144-3p mimicgroup were significantly lower than those in the NC mimic group (
P
< 0. 05), while the mRNA andprotein expression levels of PTEN in the miR-144-3p inhibitor group were significantly higher thanthose in the inhibitor NC group (
P
< 0. 05). Flow cytometry showed that the apoptosis rate of granulosa cells in the si-PTEN group was significantly lower than that in the siRNA-NC group (
P
<0. 05), while the apoptosis rate of granulosa cells in the miR-144-3p inhibitor + si-PTEN group wassignificantly lower than that in the miR-144-3p inhibitor group (
P
< 0. 05).
Conclusion
The expression level of miR-144-3p in ovarian granule cells in PCOS patients is significantly reduced,while the expression level of
PTEN
gene is significantly increased, which may have promoted theapoptosis of ovarian granule cells in PCOS patients.
Effect of SRPK1 on Malignant Progression of Triple Negative Breast Cancer Cells by Activation of the PI3K / AKT Pathway
#br#
JIANG Li, WANG Huihui, KE Longzhu, LI Gongzhuo, LUO Li
2024, 21(2): 161-165. doi:
10.3870/j.issn.1672-8009.2024.02.011
Abstract
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Objective
To explore the role of SRPK1 and PI3K / AKT signaling pathway in themalignant progression of triple negative breast cancer ( TNBC) cells.
Methods
The expressionlevel of SRPK1 in TNBC tissues and adjacent tissues was detected by immunohistochemistry. TNBCcell line MDA-MB-231 cells were divided into three groups: si
SRPK
1 group, siNC group andLY294002 group. The proliferation ability of MDA-MB-231 cells was detected by MTT assay. Transwell assay was used to analyze the invasion ability of MDA-MB-231 cells. The apoptosis rate of MDA-MB-231 cells was analyzed by flow cytometry. The expression of PI3K / AKT signalingpathway related proteins and SRPK1 protein were detected by Western blotting.
Results
The expression level of SRPK1 was increased in the TNBC tissues when compared with that in the adjacenttissues. The growth rates of MDA-MB-231 cells in the si
SRPK
1 and LY294002 groups were decreased when compared with that in the siNC group (
P
< 0. 05). The numbers of invasive MDA-MB- 231 cells in the si
SRPK
1 and LY294002 groups were significantly decreased (
P
< 0. 05). The apop
tosis rates of MDA-MB-231 cells in the si
SRPK
1 and LY294002 groups were significantly increased (
P
< 0. 05). The protein expression levels of PI3K and AKT in MDA-MB-231 cells were significantly decreased in the si
SRPK
1 and LY294002 groups (
P
< 0. 05).
Conclusion
SRPK1 is highly expressed in TNBC tissues. After inhibiting the expression of SRPK1, the proliferation and invasion ability of TNBC MDA-MB-231 cells are decreased, and the apoptosis rate is increased. This process is related to the regulation of SRPK1 on PI3K / AKT pathway.
Research Progress on Role of let-7i-5p in Tumor
#br#
OU Yong, DONG Jiaqi, WANG Ban, LI Yuanyuan, WANG Shukai, CHAO Xu
2024, 21(2): 166-170. doi:
10.3870/j.issn.1672-8009.2024.02.012
Abstract
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15
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let-7i-5p is a member of non-coding small molecule RNA (miRNA), which inhibits tumor growth, proliferation and migration through multiple targets and signaling pathways. It also has the effect of regulating tumor microenvironment to delay cancer progression and improve tumor drug resistance. This article reviews the research progress of the mechanism of let-7i-5p in liver cancer, breast cancer, colon cancer, cervical cancer, nasopharyngeal cancer, kidney cancer and glioblastoma. It is expected to explore the role that let-7i-5p can play as a new tumor marker to provide a new strategy for tumor prevention and treatment.
Advances in Gene Expression Regulatory Mechanism of
Helicobacter pylori
Virluence Factor CagA
#br#
WANG Mengmeng, YU Mengchao, WANG Lili, ZHAO Zhenyu, DONG Quanjiang
2024, 21(2): 171-175. doi:
10.3870/j.issn.1672-8009.2024.02.013
Abstract
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About half of the global population has been found to be infected with
Helicobacter pylori
(
H
.
pylori
)
, with particularly high rates in developing countries. Currently,
H
.
pylori
infection has been listed as a high-risk factor for the development of gastric cancer. The pathogenesis of
H
.
pylori
infection is believed to be associated with complex interactions between environment factors, host susceptibilities, and bacterial pathogenicity. Therefore, this article reviews the molecularmechanism of the regulation of
Helicobacter pylori
independent factor
cagA
expression, in order tobetter understand the pathogenicity of
cagA
and to provide a theoretical reference for the future prevention and treatment of diseases caused by
H
.
pylori
.
Research Progress on Glucocorticoids Induced Dysfunction of Trabecular Meshwork
#br#
REN Jing, DUAN Shichao, CUI Huiling, WANG Di, ZHAO Rumeng, LI Haijun
2024, 21(2): 176-181. doi:
10.3870/j.issn.1672-8009.2024.02.014
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Glucocorticoids (GCs) could induce the morphological changes and dysfunction oftrabecular meshwork tissues. The changes in the trabecular meshwork tissues of the glucocorticoids ( GCs) induced glaucoma is similar with those of the primary open angle glaucoma ( POAG). However, the pathogenesis of POAG is still unclear, elucidating how GCs induce morphological changes of trabecular meshwork and the increase of aqueous humor outflow resistance is beneficial for exploring the pathogenesis of POAG. The effects of GCs on trabecular meshwork are summarized in this review.
Advances in Mechanism of Hypoxia in the Progression and Treatment Tolerance of Lung Cancer
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CHEN Keming, YU Wanjun, WANG Huaying, FU Zhongming
2024, 21(2): 182-186. doi:
10.3870/j.issn.1672-8009.2024.02.015
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Hypoxia is an intrinsic feature of lung cancer. It affects the metabolism, proliferationand migration of lung cancer through genomic and proteomic regulation, and up-regulates the tolerance of lung cancer to radiotherapy and induces the resistance of lung cancer to chemotherapy and immunotherapy through complex mechanisms, which make it an important factor leading to the poor prognosis of lung cancer. This article reviews the mechanism of hypoxia in the drug resistance of lung cancer and its potential application as a therapeutic target in the clinical treatment of lung cancer.
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