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Decorin inhibits proliferation and metastasis in human bladder cancer cells by upregulating P21.

ABSTRACT: Migration of bladder cancer (BC) cells poses a substantial threat to human health. It is critical to elucidate the mechanism of BC invasion and progression for surgical treatment and the prognosis of patients. Decorin is of interest as an anticancer treatment that can play a vital role in regulating tumorigenesis. The effect of decorin expression on survival in clinical patients was screened and analyzed using bladder urothelial carcinoma data from the Cancer Genome Atlas (TCGA) database. The differential expression of transforming growth factor-β1 (TGF-β1) in tumors was compared against that of normal samples to analyze the correlation between them. MTT, flow cytometry, and Wound/Transwell assays were used to detect cell proliferation, cycle arrest, apoptosis, migration, and invasion. Analysis of TCGA data showed that decorin expression was significantly lower in bladder urothelial carcinoma samples than in normal tissues, while TGF-β1 expression did not change significantly. We found that decorin was correlated with TGF-β1 expression in bladder urothelial cancer. In addition, decorin blocked the G1/S phase by upregulating p21 protein and inhibiting the expression of TGF-β1 and MMP2, promoting the occurrence of apoptosis and inhibiting the proliferation of human BC T24 cells. Moreover, decorin increased the adhesion of tumor cells in vitro, and effectively inhibited cell metastasis. Decorin regulated the expression of TGF-β1 and MMP2 through p21 protein, promoted apoptosis and adhesion, and inhibited the proliferation and metastasis of BC cells.

SUBMITTER: Chen H

PROVIDER: S-EPMC9239591 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Knockdown of SLC35F2 Inhibits the Proliferation and Metastasis of Bladder Cancer Cells.

Project description:Background:Many studies have shown that solute carrier family 35 member F2 (SLC35F2) plays a key role in the biological processes of multiple cancers. However, there have been no reports on the role of SLC35F2 in the occurrence and development of bladder cancer (BC). Methods:SLC35F2 expression data and clinical and prognostic information from BC patients were obtained from databases. SLC35F2 expression in BC was verified by quantitative real-time PCR (qRT-PCR). The influence of SLC35F2 knockdown on the proliferation, apoptosis, migration and invasion in the 5637 and T24 cell lines was studied, and tumor formation experiments were performed in nude mice. Gene set enrichment analysis (GSEA) was used to predict the pathways and functions of SLC35F2 in BC. Results:SLC35F2 was highly expressed in BC tissues and was associated with invasiveness and T stage in BC patients. SLC35F2 knockdown can inhibit the proliferation, migration and invasion of BC cells and can promote apoptosis. SLC35F2 knockdown significantly reduced tumorigenesis in nude mice. GSEA showed that BC, pathways in cancer, apoptosis and the P53 signaling pathway were significantly enriched in SLC35F2 high expression phenotype. Conclusion:SLC35F2 can promote malignant progression and is a potential therapeutic target in BC.

| S-EPMC6911351 | biostudies-literature

SNHG18 inhibits bladder cancer cell proliferation by increasing p21 transcription through destabilizing c-Myc protein.

Project description:BackgroundLong non-coding RNAs (lncRNAs) have been confirmed to play important roles in various cancers including bladder cancer (BC). The precise expression pattern of lncRNA small nucleolar RNA host gene 18 (SNHG18) in BC and its mechanisms of action have not been fully explored.Materials and methodsThe expression of SNHG18 was evaluated by RT-qPCR in bladder cancer clinical samples and human bladder cancer cell lines, and stable cell lines overexpressing SNHG18 were constructed. The effect of SNHG18 on the proliferation of bladder cancer cells was detected by soft agar colony formation test, ATP activity test and subcutaneous tumorigenesis model in nude mice. The specific mechanism of SNHG18 inhibition of bladder cancer proliferation was studied by flow cytometry, western blotting, dual luciferase reporter gene assay and protein degradation assay.ResultsWe found that SNHG18 is significantly downregulated in BC tissues and cell lines. Kaplan-Meier analysis showed that SNHG18 expression is positively correlated with survival in BC patients. Ectopic overexpression of SNHG18 significantly inhibited the proliferation of BC cells in vitro and in vivo. Further mechanistic investigations demonstrated that SNHG18 inhibited c-Myc expression by modulating the ubiquitination-proteasome pathway and that c-Myc is the critical transcription factor that mediates SNHG18 inhibition of BC growth by directly binding to the p21 promoter, which was attributed with significant p21 accumulation.ConclusionsSNHG18 promotes the transcription and expression of p21 by inhibiting c-Myc expression, leading to G0-G1 arrest and inhibiting the proliferation of bladder cancer cells. These findings highlight a novel cell cycle regulatory mechanism involving the SNHG18/c-Myc/p21 pathway in BC pathogenesis and could potentially lead to new lncRNA-based diagnostics and/or therapeutics for BC.

| S-EPMC10018893 | biostudies-literature

Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells.

Project description:B cell-specific moloney murine leukemia virus integration site 1 (BMI1) is a transcriptional repressor of polycomb repressive complex 1, which is involved in the proliferation, senescence, migration, and tumorigenesis of cancer. Experimental researchers have convincingly linked BMI1 to tumorigenesis. However, there is no study about the issue on the role of BMI1 in the proliferation, apoptosis, and migration of bladder cancer. To address this question, we examined the expression of BMI1 in bladder cancer tissues and used siRNA to knockdown BMI1 expression in bladder cancer T24 cells. Then we tested the cell proliferation by CCK8 assay and soft agar colony formation assay, apoptosis by flow cytometry assay, and cell invasiveness by transwell migration assay. Our results revealed that BMI1 promoted proliferation, migration, invasion, and progression in bladder cancer. Over-expression of BMI1 was correlated with tumor clinic-pathological features. BMI1 siRNA effectively inhibited bladder cancer cell proliferation and migration in vitro, and it promoted bladder cancer invasion, maybe by causing epithelial-to-mesenchymal transition. Our findings suggested that BMI1 may represent a novel diagnostic marker and a therapeutic target for bladder cancer, and deserves further investigation.

| S-EPMC3771375 | biostudies-literature

RUNX3 Inhibits the Invasion and Metastasis of Human Colon Cancer HT-29 Cells by Upregulating MMP-2/9.

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| S-EPMC7063181 | biostudies-literature

ESE3 Inhibits Pancreatic Cancer Metastasis by Upregulating E-Cadherin.

Project description:The ETS family transcription factor ESE3 is a crucial element in differentiation and development programs for many epithelial tissues. Here we report its role as a tumor suppressor in pancreatic cancer. We observed drastically lower ESE3 expression in pancreatic ductal adenocarcinomas (PDAC) compared with adjacent normal pancreatic tissue. Reduced expression of ESE3 in PDAC correlated closely with an increase in lymph node metastasis and vessel invasion and a decrease in relapse-free and overall survival in patients. In functional experiments, downregulating the expression of ESE3 promoted PDAC cell motility and invasiveness along with metastasis in an orthotopic mouse model. Mechanistic studies in PDAC cell lines, the orthotopic mouse model, and human PDAC specimens demonstrated that ESE3 inhibited PDAC metastasis by directly upregulating E-cadherin expression at the level of its transcription. Collectively, our results establish ESE3 as a negative regulator of PDAC progression and metastasis by enforcing E-cadherin upregulation. Cancer Res; 77(4); 874-85. ©2016 AACR.

| S-EPMC5313376 | biostudies-literature

A New Double Stranded RNA Suppresses Bladder Cancer Development by Upregulating p21 (Waf1/CIP1) Expression.

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| S-EPMC4396018 | biostudies-literature

Long non-coding RNA Loc490 inhibits gastric cancer cell proliferation and metastasis by upregulating RNA-binding protein Quaking.

Project description:Gastric cancer (GC) is one of the most common malignant tumor types worldwide. Long non-coding RNAs (lncRNAs) have important epigenetic effects, including altering the proliferation and metastasis of malignant tumors. We used gene chip technology to search for lncRNAs that were differentially expressed in GC and metastatic lymph node tissues compared with adjacent normal tissues. The lncRNA Loc490 and the RNA-binding protein Quaking (QKI) were downregulated in GC tissues and lymph node metastases compared with normal tissues, and the levels of these two genes correlated positively with one another. Loc490 expression correlated negatively with lymph node metastasis and vein/nerve invasion, while it correlated positively with overall and disease-free survival. In vitro, Loc490 post-translationally enhanced the expression of QKI and suppressed the expression of epithelial-mesenchymal transition-related molecules. Overexpression of Loc490 inhibited GC cell proliferation, invasion and metastasis and exerted strong antitumor effects in vivo, while silencing of QKI antagonized these effects. A potential binding site between Loc490 and QKI was detected through bioinformatics analysis and confirmed through RNA immunoprecipitation and mutant analyses. Our results suggest that lncRNA Loc490 inhibits GC cell proliferation and metastasis by upregulating RNA-binding protein QKI.

| S-EPMC7521539 | biostudies-literature

Recombinant human decorin suppresses liver HepG2 carcinoma cells by p21 upregulation.

Project description:BACKGROUND: Decorin is a multifunctional molecule of the extracellular matrix and impedes different kinds of tumor cell growth, but the role and molecular mechanism by which decorin inhibits HepG2 cells is not fully understood. Our objective was to construct recombinant human decorin (pcDNA3.1-DCN) and to explore the mechanism by which it inhibits HepG2 cells. METHODS: This experiment was divided into three groups, ie, a control group, an empty vector group, and a pcDNA3.1-DCN group. pcDNA3.1-DCN was constructed using recombinant DNA technology, and the vector for pcDNA3.1-DCN and pcDNA3.1 was then transfected into HepG2 cells using Lipofectamine 2000. RESULTS: Compared with cells in the control group and in the empty vector group, growth of cells in the pcDNA3.1-DCN group was significantly suppressed, the ratios of cells in the G0/G1 phases and proportion of early apoptotic cells were significantly increased, and the level of p21(WAF1/CIP1) (p21) protein was markedly upregulated (P < 0.05). However, there was no significant difference among the three groups in p53 protein expression (P > 0.05). CONCLUSION: The pcDNA3.1-DCN vector was successfully constructed and transfected into HepG2 cells, and decorin overexpression suppressed the growth of HepG2 cells by upregulation of p21 via a p53-independent pathway.

| S-EPMC3422087 | biostudies-other

DT-13 Inhibits Proliferation and Metastasis of Human Prostate Cancer Cells Through Blocking PI3K/Akt Pathway.

Project description:DT-13, a saponin monomer 13 from the dwarf lilyturf tuber, was reported to exhibit anti-inflammatory, hepatoprotective, cardioprotective as well as antitumor activities in a number of tumor cells. Prostate cancer is the second leading cause of cancer death in males, discovery of novel antitumor drug for therapy of prostate cancer is expected. Aiming to evaluate whether DT-13 could become a candidate to treat prostate cancer, we recently investigated the antitumor effect of DT-13 on human prostate cancer cells and the underlying mechanism. DT-13 was found to effectively inhibit proliferation and metastasis of prostate cancer PC3 and DU145 cell lines in a dose-dependent manner. Treatment by DT-13 resulted in a mitochondria-mediated apoptosis, which was accompanied by the chromatin condensation and nuclear shrinkage in the prostate cancer cells. Moreover, DT-13 caused remarkable upregulation of Bax, Bad, Cytochrome C, cleaved -caspase 3, -caspase 9 and -PARP, in contrast to the downregulation of Bcl-2. Nevertheless, no obvious change in intracellular ROS level was observed after DT-13 treatment. We further demonstrated that DT-13 could inhibit PC3 cell metastasis in which suppression of Integrinβ1 and MMP2/9 might be involved. Western blot analysis indicated DT-13 significantly decreased the phosphorylation of PDK1, Akt, mTOR as well as p70S6K, suggesting the pro-apoptotic and anti-metastatic effects of DT-13 on prostate cancer cells might be attributed to the blockade of PI3K/Akt pathway. Collectively, our findings suggest DT-13 is worthy of further investigation as a drug candidate for the treatment of prostate cancer.

| S-EPMC6292965 | biostudies-literature

ACT001 inhibits the proliferation of non-small cell lung cancer cells by upregulating NKTR expression.

Project description:BackgroundLung cancer, the primary cause of cancer-related deaths worldwide, is diagnosed at an advanced stage and has a poor prognosis. Non-small cell lung cancer (NSCLC) is a major histological type of lung malignancy. This study investigated the effect of ACT001, a novel sesquiterpene lactone derivative, on the proliferation of NSCLC cells and explored the underlying mechanism.MethodsThe effect of ACT001 on cell proliferation was examined by clone formation and MTT assay. Differentially expressed genes and enrichment pathways were analyzed by RNA-seq. Flow cytometry and cell cycle-related protein expression analysis were performed to study the cell cycle. Phosphorylated AKT was detected to explore the mechanism in natural killer cell triggering receptor (NKTR) KD cells with AKT activator and/or inhibitor. The therapeutic effect of ACT001 in vivo was studied in the xenograft tumor model.ResultsACT001 inhibited the proliferation and G1/S transition in NSCLC cell lines. By RNA-seq analysis, NKTR may be the target of ACT001. Moreover, knockdown NKTR promoted cell proliferation and reversed the effects of ACT001. In addition, ACT001 inhibited AKT phosphorylation, but NKTR knockdown promoted AKT phosphorylation.ConclusionOur results suggested NKTR may be the target of ACT001 in NSCLC. ACT001 holds promise as a novel method for the treatment of NSCLC.

| S-EPMC9200889 | biostudies-literature

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