MiR‐205 suppresses tumor growth, invasion, and epithelial‐mesenchymal transition by targeting SEMA4C in hepatocellular carcinoma

Lu, Jiong; Lin, Yixin; Li, Fuyu; Ye, Hui; Zhou, Rongxing; Jin, Yu; Li, Bei; Xiong, Xian‐Ze; Cheng, Nan-Sheng

doi:10.1096/fj.201800113r

Cited by 26 publications

(26 citation statements)

References 38 publications

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“…miR-205 can inhibit the proliferation and migration of tumor cells by targeting RUNX2 in pancreatic cancer (18). Lu et al (19) confirmed that the expression of miR-205 in HCC cells decreased, which could inhibit the migration and invasion of HCC cells. miR-205 may become a therapeutic target for HCC.…”

Section: Discussionmentioning

confidence: 97%

Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

et al. 2020

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This study explored the target of miR-205 and the effect of miR-205 on the proliferation and migration regulating its target in thyroid cancer cells (TC). Twenty-five pairs of TC and adjacent tissues were collected after surgical resection. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect the expression of miR-205 in TC tissues and cells (SW579, B-CPAP, TPC-1, WRO). SW579 cells were transfected with miR-205 mimic, and SW579 cells with overexpression of miR-205 were constructed. The effects of miR-205 overexpression on the proliferation and migration of SW579 cells were observed by cell counting kit-8 (CCK-8) and Transwell assays, respectively. Luciferase reporter assay was further used to look for the target of miR-205 and to study the mechanism of miR-205 in the proliferation and migration of TC cells. Compared with normal tissues and cells, the expression of miR-205 was significantly reduced in TC tissues (t=3.47, P= 0.031) and cells (t=5.41, P= 0.016). Overexpression of miR-205 inhibited the proliferation (t=4.12, P= 0.035) and migration (t= 4.47, P= 0.027) of SW579 cells. Luciferase reporter assays found that CCNB2 was a target gene of miR-205 (t= 4.63, P= 0.024), qRT-PCR and western blot assays confirmed there was negatively correlation between CCNB2 and miR-205 (t=3.55, P= 0.029; t=2.86, P= 0.043). CCNB2 overexpression reversed the inhibition of miR-205 on the proliferation (t=3.70, P=0.031) and migration (t=4.12, P=0.022) of SW579 cells. In conclusion, miR-205 inhibits the proliferation and migration of TC cells by targeting CCNB2, which may be a potential target of TC therapy.

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Section: Discussionmentioning

confidence: 97%

Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

et al. 2020

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“…192 Moreover, miR-205 inhibited tumor growth, invasion, and EMT via targeting semaphorin 4C in hepatocellular carcinoma. 193 Furthermore, the upregulation of miR-183-5p induced apoptosis and inhibited EMT, proliferation, invasion, and migration by the downregulation of ezrin in human endometrial cancer cells. 194 Collectively, EMT is inhibited by many miRNAs, including miR-145, miR-497, miR-145-5p, miR-138, miR-200a, miR-200b, miR-655, miR-30-5p, and miR-32.…”

Section: Ras Signaling Pathwaymentioning

confidence: 99%

“…For example, miRNA‐497/Wnt3a/c‐Jun regulated growth and EMT, and miR‐497 served as a tumor suppressor in glioma cells . Moreover, miR‐205 inhibited tumor growth, invasion, and EMT via targeting semaphorin 4C in hepatocellular carcinoma . Furthermore, the upregulation of miR‐183‐5p induced apoptosis and inhibited EMT, proliferation, invasion, and migration by the downregulation of ezrin in human endometrial cancer cells .…”

Section: Small Molecules Against Emtmentioning

confidence: 99%

Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

Feng

Chen

Vaziri

et al. 2019

Medicinal Research Reviews

102

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Tissue fibrosis and cancer both lead to high morbidity and mortality worldwide; thus, effective therapeutic strategies are urgently needed. Because drug resistance has been widely reported in fibrotic tissue and cancer, developing a strategy to discover novel targets for targeted drug intervention is necessary for the effective treatment of fibrosis and cancer. Although many factors lead to fibrosis and cancer, pathophysiological analysis has demonstrated that tissue fibrosis and cancer share a common process of epithelial‐mesenchymal transition (EMT). EMT is associated with many mediators, including transcription factors (Snail, zinc‐finger E‐box‐binding protein and signal transducer and activator of transcription 3), signaling pathways (transforming growth factor‐β1, RAC‐α serine/threonine‐protein kinase, Wnt, nuclear factor‐kappa B, peroxisome proliferator‐activated receptor, Notch, and RAS), RNA‐binding proteins (ESRP1 and ESRP2) and microRNAs. Therefore, drugs targeting EMT may be a promising therapy against both fibrosis and tumors. A large number of compounds that are synthesized or derived from natural products and their derivatives suppress the EMT by targeting these mediators in fibrosis and cancer. By targeting EMT, these compounds exhibited anticancer effects in multiple cancer types, and some of them also showed antifibrotic effects. Therefore, drugs targeting EMT not only have both antifibrotic and anticancer effects but also exert effective therapeutic effects on multiorgan fibrosis and cancer, which provides effective therapy against fibrosis and cancer. Taken together, the results highlighted in this review provide new concepts for discovering new antifibrotic and antitumor drugs.

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“…miR-2392 suppresses metastasis and EMT by targeting MAML3 and WHSC1 in gastric cancer (6). miR-205 suppresses tumor growth, invasion, and EMT by targeting SEMA4C in hepatocellular carcinoma (7). However, the implication of miRNAs in colon cancer remains to be clarified.…”

mentioning

confidence: 99%

miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

Sun

Liu²,

Lin

et al. 2019

FASEB j.

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The epithelial‐mesenchymal transition (EMT) is crucial for cancer progression. Evidence has shown that miR‐22 and miR‐214 play a key role in colon cancer progression; however, the underlying mechanism remains to be known. The effects of miR‐22 and miR‐214 on EMT are contradictory in different cancers, and whether miR‐22 and miR‐214 are involved in the colon cancer EMT process needs to be elucidated. In this study, we evaluated the exact role and the regulation mechanism of miR‐22 and miR‐214 in colon cancer. After transfection with miR‐22 expression vector, the cell proliferation and migration capacity of HCT116 and RKO cells were significantly suppressed. Also, E‐cadherin was increased and vimentin was decreased by miR‐22 overexpression. Similar effects were also observed after miR‐214 expression vector transfection. Dual‐lucif erase reporter confirmed that BCL9L is the target gene of both miR‐22 and miR‐214. Silencing of BCL9L inhibits cell proliferation and migration, and the expression of E‐cadherin and vimentin was also altered by BCL9L knockdown, which was consistent with miR‐22 or miR‐214 transfection. Furthermore, miR‐22 and miR‐214 inhibited tumor growth in nude mice. Moreover, although the association between BCL9L's lower expression and longer survival time was statistically nonsignificant, a trend existed; further studies in a larger cohort are needed. Collectively, these data suggest that miR‐22 and miR‐214 inhibit cell proliferation, migration, and EMT of colon cancer, most likely by targeting BCL9L.—Sun, R., Liu, Z., Han, L., Yang, Y., Wu, F., Jiang, Q., Zhang, H., Ma, R., Miao, J., He, K., Wang, X., Zhou, D., Huang, C. miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signliang in colon cancer. FASEB J. 33, 5411–5424 (2019). http://www.fasebj.org

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MiR‐205 suppresses tumor growth, invasion, and epithelial‐mesenchymal transition by targeting SEMA4C in hepatocellular carcinoma

Cited by 26 publications

References 38 publications

Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

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