CDCA5 is a potent therapeutic target of clear cell renal cell carcinoma
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Abstract Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer in adult, and patients with advanced ccRCC are facing limited treatment options. Cell division cycle associated 5 (CDCA5), a key regulator for segregating sister chromatids in cell cycle, has been increasingly reported for a potential therapeutic target in multiple human cancers. However, the functional roles of CDCA5 in ccRCC remain uncertain. Here we identified that CDCA5 expression was frequently upregulated in ccRCC tumors and significantly associated with poor prognosis of ccRCC patients. To investigate the role of CDCA5 in ccRCC progression, loss function cell models were established. Knockdown of CDCA5 remarkably suppressed ccRCC cell proliferation and migration ability, and also induced cell apoptosis in vitro. In addition, the significance of CDCA5 in ccRCC was further demonstrated in a mouse xenograft model. Silencing of CDCA5 drastically inhibited in vivo tumorigenicity of ccRCC cells. Mechanically, we identified CDCA5 may cooperate with EEF1A1 to promote the tumorigenic phenotype of ccRCC. Overall, our results revealed the significant functional role of CDCA5 in ccRCC progression, which may pave a way for the development of new treatment strategies for ccRCC treatment.Objective:To assess the effect of Uncarinic Acid E(UAE) on the HepG2 cell,a human hepatoma cell line,and investigate the mechanism of induced HepG2 cell death.Methods:Cytotoxic effect was examined by MTT assay;ultrastructure of HepG2 cell was observated by electronic microscopy;while the cell cycle distribution was determined by flow cytometric analysis.Results:Cell growth of HepG2 cells was inhibited by UAE,electron microscope analysis showed that UAE initiated apoptosis in HepG2 cell,which is also obtained by the result of flow cytometric analysis,and the cell cycle arrest occurred in G0/G1 phase.Conclusion:Uncarinic Acid E showed an anti-proliferation effect and induced apoptosis of HepG2 cell in vitro.
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Objective To investigate the proliferation inhibition and apoptosis of human liver cancer Bel-7402cell line induced by GA in vetro.Methods The cell proliferation was determined by MTT assay.The cell apoptosis and cell cycle were analyzed by flow cytometry.The expressions of Bcl-2and Bax mRNA and protein were detected by RT-PCR and Western blot,respectively.Results GA inhibited the proliferation of Bel-7402cells in the does-and time-dependent manners.As the concentration of GA increased,the apoptosis rate of the cells increased.Meanwhile,GA induced G2 /M cell cycle arrest.The expressions of Bax mRNA and protein were upregulated while those of Bcl-2 were downregulated.Conclusion GA inhibits cell proliferation and enhances cell apoptosis,which may be related to the upregulation of Bax gene expression,downregulation of Bcl-2gene expression and the cell cycle arrest.
Gambogic acid
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In this study, we found miR-362-5p was upregulated in bladder cancer tissues and we predicted that QKI is potential a target of miR-362-5p and MBNL1-AS1 might be able to directly bind with miR-362-5p. We attempted to evaluate whether miR-362-5p could play its roles in bladder cancer through regulating QKI (quaking) and whether the expression and function of miR-362-5p could be mediated by lncRNA MBNL1-AS1. We performed the gain- and loss- function experiments to explore the association between miR-362-5p expression and bladder cancer proliferation. In vivo, the nude mice were injected with miR-362-5p knockdown SW780 cells to assess the effects of miR-362-5p on tumor growth. The results showed upregulation of miR-362-5p promoted cell proliferation of bladder cancer cells. MBNL1-AS1 and QKI could directly bind with miR-362-5p, and knockdown of MBNL1-AS1 or QKI could abrogate the regulatory effects of miR-362-5p on bladder cancer cell proliferation. Furthermore, downregulation of miR-362-5p inhibited bladder tumor growth and increased QKI expression. Our data unveiled that miR-362-5p may play an oncogenic role in bladder cancer through QKI and MBNL1-AS1 might function as a sponge to mediate the miR-362-5p expression and function.
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Objective To explore the effect of Tanshinone ⅡA on cell proliferation,apoptosis and cell cycle of fibroblasts derived from keloid.Methods Fibroblasts derived from keloid were cultured with different concentration of Tanshinone ⅡA(0 μg/mL,50 μg/mL,100 μg/mL and 200 μg/mL) in vitro.CCK-8 was used to detect cell proliferation,and flow cytometry was used to analyze cell apoptosis,cell cycle at the different time.Results Cell proliferation of fibroblasts derived from keloid was decreased,apoptosis at the early phase was increased,and cell cycle in G0/G1 phase was arrested by different concentration of Tanshinone ⅡA with different intervention time(P0.001),especially in 200 μg/mL group.Variance analysis showed that those differences have statistical significance.Conclusion Tanshinon ⅡA can suppress cell proliferation,induce cell apoptosis and arrest cell cycle of fibroblasts derived from keloid.The effect of Tanshinone ⅡA was affected by different concentration and different intervention time.
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miR‑886‑3p has been discovered to be involved in the oncogenesis, progression and metastasis of several types of human cancer. The aim of the present study was to identify the biological function of miR‑886‑3p in clear cell renal cell carcinoma (ccRCC) and to determine its possible molecular mechanisms. miR‑886‑3p was found to be significantly upregulated in ccRCC tissues (P<0.05), in accordance with a previous sequencing result. Functional experiments revealed that forced downregulation of miR‑886‑3p significantly inhibited cellular migration, suppressed cell proliferation and induced cell apoptosis of renal cancer cells. Paired‑like homeodomain 1 (PITX1), which has been identified as a tumor suppressor, was found to be downregulated in ccRCC tissues and identified as a target gene of miR‑886‑3p. Further experiments demonstrated that the protein level, and not the mRNA level, of PITX1 was significantly decreased or increased when miR‑886‑3p was upregulated or downregulated, respectively, indicating that miR‑886‑3p acted as an oncogene by directly regulating the protein expression of PITX1 at a post‑transcriptional level. In conclusion, this study revealed that miR‑886‑3p was upregulated in ccRCC and was involved in cellular migration, proliferation and apoptosis of renal cancer cells by directly targeting the tumor suppressor gene, PITX1.
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Abstract Objective: Our study aims to investigate the mechanism of the miR-129-5p/SPN axis in clear cell renal cell carcinoma (ccRCC), providing a novel direction for the targeted therapy of ccRCC. Methods: Bioinformatics methods were implemented to find the differentially expressed genes (DEGs) associated with ccRCC from TCGA database. qRT-PCR was performed to detect miR-129-5p and SPN mRNA expression, while western bot was carried out for the detection of protein expression of SPN. Bioinformatics analysis was used to predict the binding sites of miR-129-5p on SPN 3’UTR, while dual-luciferase assay was conducted to verify their binding relationship. CCK-8 assay, colony formation assay, wound healing assay and Transwell assay were employed to measure ccRCC cell proliferative ability, cell formation ability, cell migratory and invasive abilities. Flow cytometry was implemented to assess cell cycle and apoptosis. Results: miR-129-5p exhibited a significantly down-regulated expression level in ccRCC, while SPN showed a remarkably up-regulated expression level. Overexpressed miR-129-5p inhibited ccRCC cell proliferative, invasive and migratory capacities while induced cell cycle arrest in G0/G1 phase and promoted cell apoptosis. Dual-luciferase assay confirmed that there was a binding relationship between miR-129-5p and SPN. Moreover, overexpressed miR-129-5p remarkably reduced SPN expression in cancer cells, weakened the promoting effect of SPN on cell proliferation, migration, invasion and cell cycle progress, and led to enhanced cell apoptotic activity. Conclusion: Our study proves the regulatory effect of the miR-129-5p/SPN axis in ccRCC, and provides a novel potential target for precise treatment of patients with ccRCC.
G1 phase
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Abstract Objective Our study aims to investigate the mechanism of the miR-129-5p/SPN axis in clear cell renal cell carcinoma (ccRCC), providing a novel direction for the targeted therapy of ccRCC. Methods Bioinformatics methods were implemented to find the differentially expressed genes (DEGs) associated with ccRCC from TCGA database. qRT-PCR was performed to detect miR-129-5p and SPN mRNA expression, while western bot was carried out for the detection of protein expression of SPN. Bioinformatics analysis was used to predict the binding sites of miR-129-5p on SPN 3’UTR, while dual-luciferase assay was conducted to verify their binding relationship. CCK-8 assay, colony formation assay, wound healing assay and Transwell assay were employed to measure ccRCC cell proliferative ability, cell formation ability, cell migratory and invasive abilities. Flow cytometry was implemented to assess cell cycle and apoptosis. Results miR-129-5p exhibited a significantly down-regulated expression level in ccRCC, while SPN showed a remarkably up-regulated expression level. Overexpressed miR-129-5p inhibited ccRCC cell proliferative, invasive and migratory capacities while induced cell cycle arrest in G0/G1 phase and promoted cell apoptosis. Dual-luciferase assay confirmed that there was a binding relationship between miR-129-5p and SPN. Moreover, overexpressed miR-129-5p remarkably reduced SPN expression in cancer cells, weakened the promoting effect of SPN on cell proliferation, migration, invasion and cell cycle progress, and led to enhanced cell apoptotic activity. Conclusions Our study proves the regulatory effect of the miR-129-5p/SPN axis in ccRCC, and provides a novel potential target for precise treatment of patients with ccRCC.
G1 phase
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Renal pelvis cancer (RPC) is rare with unclear pathogenesis. Resveratrol (RSV) also plays a beneficial role in preventing chronic diseases related to inflammation. But its effect on RPC cells has not been reported. RPC cells were cultured and treated with resveratrol for 48 hours followed by analysis of cell proliferation, apoptosis and cell cycle, and miR-30a-5p expression. The expression of miR-30a-5p effects proliferation, apoptosis and cell cycle was also assessed. After treatment, RPC cells showed upregulated miR-30a-5p, decreased cell survival and enhanced cell apoptosis rate compared with abnormal cell cycle ( P < 0.05), and the effect was more significant with the increase in concentration ( P < 0.05). The miR-30a-5p target gene is AVEN. miR-30a-5p downregulation can reverse its effect on RPC cells ( P < 0.05). Resveratrol treatment on RPC cells can upregulate miR-30a-5p, inhibite cell proliferation, promotes apoptosis, and changes cell cycle.
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Objective To dissect the functioning mode of miR-645 on renal clear cell carcinoma cell metastasis and growth, and provide therapeutic targets for renal clear cell carcinoma. Patients and methods Quantitative Real-time PCR (qRT-PCR) assay was employed to detect miR-645 expression level. Wound healing assay and transwell assay were performed to investigate metastasis capacity of renal clear cell carcinoma cells. Cell Counting Kit 8 (CCK8) assay was incorporated to assess cell proliferation capacity. Flow cytometry was used to identify cell apoptosis and cell cycle distribution. Protein levels were assessed by Western blotting assay. The target gene was predicted and verified by bioinformatics analysis and luciferase assay. Results MiR-645 was upregulated in renal clear cell carcinoma tissues when compared with para-carcinoma tissues (n=32). Downregulated miR-645 could attenuate cell migration and invasion capacities, as well as inhibited cell proliferation capacity, promoted cell apoptosis and cell cycle arrest at G0/G1 phase. GK5 was chosen as the target gene of miR-645 by bioinformatics analysis and luciferase reporter assay. Moreover, silence of GK5 could rescue tumor suppression role of downregulated miR-645 on renal clear cell carcinoma metastasis. Conclusions Knockdown of miR-645 exerted tumor-suppressive effects on renal clear cell carcinoma metastasis and growth via targeting GK5 in vitro, which provided an innovative and candidate target for diagnose and treatment of renal clear cell carcinoma.
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Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, was found to be involved in the development and progression of several tumors. However, the role of URG11 in human non-small cell lung cancer (NSCLC) has not yet been determined. Therefore, the aim of the present study was to explore the role of URG11 in human NSCLC. Our results found that URG11 was highly expressed in human NSCLC tissues compared with matched normal lung tissues, and higher levels were found in NSCLC cell lines in comparison to the normal lung cell line. Moreover, we also found that knockdown of URG11 significantly inhibited proliferation, migration/invasion of NSCLC cells, as well as suppressed tumor growth in vivo. Furthermore, knockdown of URG11 suppressed the expression of β-catenin, c-Myc, and cyclin D1 in NSCLC cells. Taken together, the study reported here provided evidence that URG11 downregulation suppresses proliferation, invasion, and β-catenin expression in NSCLC cells. Thus, URG11 may be a novel potential therapeutic target for NSCLC.
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