Silencing of miR-193a-5p increases the chemosensitivity of prostate cancer cells to docetaxel

Yang, Zhan; Chen, Jin-Suo; Wen, Jin‐Kun; Gao, Huimin; Zheng, Bin; Qu, Chun-Ying; Liu, Kailong; Zhang, Manli; Gu, Junfei; Li, Jingdong; Zhang, Yanping; Li, Wei; Wang, Xiaolu; Zhang, Yong

doi:10.1186/s13046-017-0649-3

Cited by 78 publications

(91 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The transfection used Lipofectamine 2000 (Thermo Fisher Scientific, Waltham, MA, USA) according to the manufacturer's protocols as previously described by Yang et al (28). The miR-432-5p mimics, mimic negative control (NC), miR-432-5p inhibitors, inhibitor NC, RBM5-shRNAs, b-catenin short hairpin RNA (shRNA), and negative controls were purchased from GenePharma (Shanghai, China).…”

Section: Cell Transfectionmentioning

confidence: 99%

“…All animal studies were approved by the Institutional Animal Care and Use Committee of Hebei Medical University (20080026) and were made to minimize suffering. Xenograft model was performed as previously described (28,33). Male BALB/c nude mice at 4-6 wk of age (18-22 g) were purchased from Vital River Laboratory Animal Technology (Beijing, China).…”

Section: Xenograft Animal Modelmentioning

confidence: 99%

“…Five-micrometers paraffin-embedded cross-sections of tissues were subjected to immunofluorescence staining as previously described by Yang et al (28). Sections were deparaffinized with xylene, rehydrated, and preincubated with 10% normal goat serum (710027; Seracare, Milford, MA, USA) followed by incubation with the following primary antibody: anti-RBM5 (19930-1-AP).…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

“…The chromatin immunoprecipitation (ChIP) assay was performed as previously described by Yang et al (28). In brief, T24 cells were treated with 1% formaldehyde for 10 min to cross-link proteins with DNA.…”

Section: Chromatin Immunoprecipitation Assaymentioning

confidence: 99%

See 3 more Smart Citations

Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/β‐catenin feedback loop

et al. 2019

Self Cite

View full text Add to dashboard Cite

RNA‐binding motif protein 5 (RBM5) acts as a tumor suppressor in various human cancers and presents with several important characteristics, such as the potentiation of apoptosis, inhibition of the cell cycle, and alternative splicing of Fas and caspase‐2 precursor mRNA. However, its role in bladder urothelial carcinoma (BUC) remains unknown. In this study, we found that RBM5 expression was significantly down‐regulated in BUC tissues when compared with the adjacent nontumor tissues. The down‐regulation of RBM5 activates ²‐catenin, which binds to the T‐cell factor/lymphocyte enhancer factor element of the miR‐432‐5p promoter and elevates the expression of miR‐432‐5p in bladder cancer cells. The up‐regulated miR‐432‐5p directly targets 3′‐UTR and depresses RBM5 expression. Thus, RBM5–miR‐432‐5p–²‐catenin forms a feedback loop in regulating bladder cancer cell apoptosis. Our findings provide evidence that the regulatory feedback loop among RBM5, miR‐432‐5p, and Wnt–²‐catenin is responsible for the progress of bladder cancer cells.—Zhang, Y.‐P., Liu, K.‐L., Wang, Y.‐X., Yang, Z., Han, Z.‐W., Lu, B.‐S., Qi, J.‐C, Yin, Y.‐W., Teng, Z.‐H., Chang, X.‐L., Li, J.‐D., Xin, H., Li, W. Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/²‐catenin feedback loop. FASEB J. 33, 10973–10985 (2019). http://www.fasebj.org

show abstract

Section: Cell Transfectionmentioning

confidence: 99%

Section: Xenograft Animal Modelmentioning

confidence: 99%

Section: Immunofluorescence Stainingmentioning

confidence: 99%

Section: Chromatin Immunoprecipitation Assaymentioning

confidence: 99%

See 2 more Smart Citations

Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/β‐catenin feedback loop

et al. 2019

Self Cite

View full text Add to dashboard Cite

show abstract

“…[7][8][9] Functional studies have confirmed that miRNA participates in various biological processes including cell development, differentiation, and proliferation. [15][16][17][18][19][20] Although miR-193a-5p has been proven to inhibit cell proliferation and colony formation, induce cell-cycle arrest in the G0/G1 phase and suppress tumor cell invasion, the function and the underlying mechanism of miR-193a-5p in GBM remain elusive. 14 According to previous reports, microRNA-193a-5p (miR-193a-5p) is a tumor suppressor which is lowly expressed in multiple cancers including gastric cancer, breast cancer, prostate cancer, non-small cell lung cancer, osteosarcoma, and ovarian cancer.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐193a‐5p exerts a tumor suppressor role in glioblastoma via modulating NOVA1

Jin

Wang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Background and Objectives Glioblastoma (GBM) is the most common and lethal of intracranial tumors, which is characterized by extensive proliferation and the diffused invasion of tumor cells. MicroRNA‐193a‐5p (miR‐193a‐5p) have been demonstrated previously as a functional suppressor in the development and progression of various cancers. The current study aimed to investigate whether miR‐193a‐5p influences cell proliferation and migration through the mitogen‐activated protein kinase/extracellular signal‐regulated kinase signaling pathway by targeting neuro‐oncological ventral antigen 1 (NOVA1) in glioblastoma. Materials and Methods The miR‐193a‐5p expression was detected by quantitative real‐time polymerase chain reaction assay in GBM tissues and cell lines. Cell Counting Kit‐8 assay, colony formation analysis, wound‐healing, and transwell invasion assays were performed to evaluate cell proliferation, colony formation, migration, and invasion, respectively. Western blot analysis and luciferase reporter gene assay were performed to verify the downstream target gene of miR‐193a‐5p. Results The expression of miR‐193a‐5p was significantly downregulated in GBM tissues and cell lines. Kaplan‐Meier analysis showed that patients with low miR‐193a‐5p expression had a shorter disease‐free survival (P < 0.05). Functionally, miR‐193a‐5p overexpression dramatically suppressed the proliferation, colony formation, migration, and invasion in glioma cells. Bioinformatics prediction and a luciferase assay confirmed that NOVA1 was a direct functional target of miR‐193a‐5p. Moreover, ectopic expression of NOVA1 could partially reverse the inhibitory effects of miR‐193a‐5p on glioma cell proliferation, colony formation, migration, and invasion. NOVA1 overexpression abrogated the inhibitory effect of miR‐193a‐5p on the PTEN/PI3k/AKT pathway. Conclusion Taken together, our findings suggested that miR‐193a‐5p functions as a tumor suppressor in glioma cells by directly targeting NOVA1.

show abstract

RETRACTED: LINC01224 accelerates malignant transformation via MiR‐193a‐5p/CDK8 axis in gastric cancer

et al. 2021

View full text Add to dashboard Cite

Background Gastric cancer (GC) is a malignant tumor with a significantly high mortality rate, yet, its pathogenesis is not fully understood. Bioinformatics predicted that LINC01224 is highly expressed in stomach adenocarcinoma (STAD), and showed that LINC01224 adsorbed miR‐193a‐5p to target CDK8. Therefore, this study intended to verify the effect of the LINC01224/miR‐193a‐5p/CDK8 axis on the biological behavior of gastric cancer. Methods Expressions of LINC01224, miR‐193a‐5p, CDK8, apoptosis‐, and EMT‐related genes were analyzed using the GEPIA website, RT‐qPCR, in situ hybridization, and Western blot as needed. Bioinformatics and dual luciferase assay were used to evaluate the relationship between LINC01224, miR‐193a‐5p, and CDK8. Functional experiments and rescue experiments (MTT assay, flow cytometry, wound healing assay, and Transwell) were conducted to detect the effects of the above genes on the biological characteristics of GC cells. Tumorigenesis assay was used to verify the results of in vitro experiments. Results LINC01224 adsorbed miR‐193a‐5p to target and upregulate CDK8. The expressions of LINC01224 and CDK8 were increased, while the expression of miR‐193a‐5p was decreased in GC. Overexpressed LINC01224 promoted cell viability, migration and invasion, accelerated tumor formation, attenuated apoptosis, inhibited the expressions of apoptosis‐related proteins, and promoted the expressions of EMT‐related proteins, whereas silenced LINC01224 led to the opposite effect. MiR‐193a‐5p inhibitor partially offset the effect of silenced LINC01224; interestingly, siCDK8 significantly reversed the effect of miR‐193a‐5p inhibitor on GC cells. Conclusion LINC01224 affects the biological behavior of gastric cancer by mediating miR‐193a‐5p to regulate CDK8.

show abstract

Silencing of miR-193a-5p increases the chemosensitivity of prostate cancer cells to docetaxel

Cited by 78 publications

References 52 publications

Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/β‐catenin feedback loop

Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/β‐catenin feedback loop

MicroRNA‐193a‐5p exerts a tumor suppressor role in glioblastoma via modulating NOVA1

RETRACTED: LINC01224 accelerates malignant transformation via MiR‐193a‐5p/CDK8 axis in gastric cancer

Contact Info

Product

Resources

About