Molecular mechanism of miR‐153 inhibiting migration, invasion and epithelial‐mesenchymal transition of breast cancer by regulating transforming growth factor beta (TGF‐β) signaling pathway

Wang, Jingwei; Liang, Shuhang; Xiu-qing, Duan

doi:10.1002/jcb.28230

Cited by 23 publications

(24 citation statements)

References 22 publications

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“…The present study revealed that miR-153 expression decreased in hypoxia-treated HPASMCs. It was also found that miR-153 inhibitor increased HPASMC proliferation and migration, while the miR-153 mimic reversed the increased proliferation and migration of HPASMCs induced by hypoxia, which is consistent with previous studies in cancer cells (43)(44)(45). All these data suggested that miR-153 regulated hypoxia-induced cell proliferation and migration.…”

Section: Discussionsupporting

confidence: 91%

MicroRNA‑153 attenuates hypoxia‑induced excessive proliferation and migration of pulmonary arterial smooth muscle cells by targeting ROCK1 and NFATc3

Zhao

Wang

et al. 2021

Mol Med Rep

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The aim of the present study was to explore the effect of microRNA (miR)-153 on the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) in a hypoxic condition by targeting ρ-associated, coiled-coil-containing protein kinase 1 (ROCK1) and nuclear factor of activated T cells cytoplasmic 3 (NFATc3). The right ventricular systolic pressure, right ventricular hypertrophy index, medial wall thickness and medial wall area were studied at different time-points after rats were exposed to hypoxia. Western blot analysis was used to detect ROCK1 and NFATc3 protein levels. In addition, reverse transcription-quantitative (RT-q) PCR was performed to confirm the mRNA levels of miR-153, ROCK1 and NFATc3 in human (H)PASMCs under hypoxic conditions. Transfected cells were then used to evaluate the effect of miR-153 on cell proliferation and migration abilities. The association between miR-153 and ROCK1 or NFATc3 was identified through double luciferase assays. Hypoxia induced pulmonary vascular remodeling and pulmonary arterial hypertension, which resulted from the abnormal proliferation of HPASMCs. ROCK1 and NFATc3 were the target genes of miR-153 and miR-153 mimic inhibited the protein expressions of ROCK1 and NFATc3 in HPASMCs and further inhibited cell proliferation and migration under hypoxic conditions. By contrast, the miR-153 inhibitor promoted the proliferation and migration of HPASMCs. miR-153 regulated the proliferation and migration of HPASMCs under hypoxia by targeting ROCK1 and NFATc3.

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Section: Discussionsupporting

confidence: 91%

MicroRNA‑153 attenuates hypoxia‑induced excessive proliferation and migration of pulmonary arterial smooth muscle cells by targeting ROCK1 and NFATc3

Zhao

Wang

et al. 2021

Mol Med Rep

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“…9 Moreover, Wang et al pointed out that miR-153 could regulate the TGF-β signaling pathway to repress the malignant evolution of BC cells. 10 Fkih M'hamed et al have found that the expression levels of miR-153 in TNBC and non-TNBC were similar. 33 Nevertheless, another study suggested that the expression of miR-153 was different in diverse molecular types.…”

Section: Discussionmentioning

confidence: 99%

“…6,7 Accumulating studies show that miRNAs are involved in the pathogenesis of BC in which miR-153 was aberrantly expressed. [8][9][10] Moreover, miR-153 was considered as a potential biomarker of TNBC. 11 Modes of actions and prognostic value of miR-153 in TNBC, however, have not been fully illuminated.…”

Section: Introductionmentioning

confidence: 99%

<p>Upregulation Of miR-153 Inhibits Triple-Negative Breast Cancer Progression By Targeting ZEB2-Mediated EMT And Contributes To Better Prognosis</p>

Shi

Fan

et al. 2019

OTT

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Background: Triple-negative breast cancer (TNBC) is the most malignant type of breast cancer. MicroRNAs (miRs) and their corresponding molecular targets are associated with the occurrence and development of various human malignancies. However, the roles of the microRNA-153 (miR-153) and zinc finger E-box-binding homeobox 2 (ZEB2)-induced epithelial-mesenchymal transition (EMT) in TNBC and predictive effect of miR-153 on the prognosis of TNBC have not been fully elucidated. Materials and methods: Relative miR-153 expression level was examined by RT-qPCR assay in TNBC tissues of 60 patients and TNBC cell lines (SKBR3, BT-549 and MDA-MB-231). Cell proliferation ability, invasion ability and migration ability were measured by CCK8 assay, Transwell invasion assay and wound healing assay, respectively. Luciferase reporting experiment was used to confirm that there was a miR-153-binding site in ZEB2 3ʹ-UTR. The expression of ZEB2 in tissues and its relationship with miR-153 were analyzed with immunohistochemistry method. Relative ZEB2, E-cadherin, N-cadherin and Vimentin mRNA and protein expression levels were observed with RT-qPCR and Western blot, respectively. Based on risk factors, a prognostic model was established according to the Cox proportional risk model, and the prognostic risk factors of TNBC patients were predicted and analyzed. Results: The expression of miR-153 in TNBC tissues and cells was declined (all P<0.01), and upregulation of miR-153 inhibited proliferation, invasion and migration of TNBC cells (all P<0.01). In addition, miR-153 regulated ZEB2/EMT link in TNBC, and ZEB2 overexpression reversed the tumor-suppressive effect of miR-153 in TNBC. Moreover, miR-153 was an independent predictive factor that was associated with excellent prognosis in TNBC patients. Conclusion: miR-153 may inhibit TNBC proliferation, invasion and migration by regulating ZEB2/EMT link. Therefore, miR-153 is expected to be a molecular target and prognostic marker for TNBC.

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“…miR-153 affected the progression of nasopharyngeal cancer by targeting the TGF-β2/Smad2 signaling pathway. Wang et al [14] found that the expression of miR-153 in breast cancer tissue specimens and MDA-MB-231 cells was significantly lower than that in nonmalignant counterparts. Furthermore, miR-153 inhibited migration, invasion and epithelial-mesenchymal transition of breast cancer by regulating transforming growth factor beta (TGF-β) signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Increased expression of miR-153 predicts poor prognosis for patients with prostate cancer

Zhang

Bai

et al. 2019

Medicine

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Deregulation of miR-153 has recently been observed in several common human cancer, while miR-153 serves an oncogene or tumor suppressive role in different cancer types. Previously, miR-153 has been identified to be overexpressed in prostate cancer. miR-153 played an important role in promoting proliferation of human prostate cancer cells and presented a novel mechanism of microRNA-mediated direct suppression of phosphatase and tensin homolog (PTEN) expression in prostate cancer cells. Until now, little is known about the clinical significance of miR-153 expression in prostate cancer.The miR-153 expression in 143 pairs of prostate cancer and adjacent non-cancerous prostate tissues was measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis. Student t test was conducted for intergroup comparison. Pearson correlation test was used for correlation analysis. Survival curves were carried out by the Kaplan–Meier method and evaluated using the log-rank test. Multivariable Cox proportional hazard risk regression model was performed to screen the independent factor affected the prognosis of prostate cancer patients.qRT-PCR analysis showed that the expression of miR-153 was significantly increased in the prostate cancer tissues in comparison with the adjacent noncancerous prostate tissues (P < .001). The high expression of miR-153 in prostate cancer tissues is closely correlated with aggressive clinical pathological parameters such as lymph node metastasis (P = .001); bone metastasis (P < .001); Gleason score (P < .001); and tumor-node-metastasis (TNM) stage (P < .001). Prostate cancer patients with a high expression of miR-153 had an evidently lower 5-year overall survival as compared with those with a low expression of miR-153 (P = .019). Notably, the multivariate Cox regression analysis indicated that miR-153 expression was an independent factor for predicting the 5-year overall survival of prostate cancer patients (hazard ratio [HR] = 2.481, 95% confidence interval [CI]: 1.582–10.727; P = .018).Our study demonstrated that high miR-153 expression was significantly associated with a poor overall survival independently of other factors in prostate cancer. Therefore, miR-153 may be an available biomarker for prostate cancer prognosis.

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Molecular mechanism of miR‐153 inhibiting migration, invasion and epithelial‐mesenchymal transition of breast cancer by regulating transforming growth factor beta (TGF‐β) signaling pathway

Cited by 23 publications

References 22 publications

MicroRNA‑153 attenuates hypoxia‑induced excessive proliferation and migration of pulmonary arterial smooth muscle cells by targeting ROCK1 and NFATc3

MicroRNA‑153 attenuates hypoxia‑induced excessive proliferation and migration of pulmonary arterial smooth muscle cells by targeting ROCK1 and NFATc3

<p>Upregulation Of miR-153 Inhibits Triple-Negative Breast Cancer Progression By Targeting ZEB2-Mediated EMT And Contributes To Better Prognosis</p>

Increased expression of miR-153 predicts poor prognosis for patients with prostate cancer

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