MicroRNA-183-5p Inhibits Aggressiveness of Cervical Cancer Cells by Targeting Integrin Subunit Beta 1 (ITGB1)

Zhang, Wei; Zhang, Mingkai; Liu, Lantao; Jin, Dayong; Wang, Pengyu; Hu, Jing

doi:10.12659/msm.910295

Cited by 20 publications

(14 citation statements)

References 22 publications

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“…26 suggesting that miR-183-5p significantly inhibited migration and invasion in cervical cancer cells. 38 It was also shown that increased expression of miR-183-5p promoted apoptosis and suppressed the EMT, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin, a membrane-cytoskeleton linker protein. 39 We also showed that induction of miR-183-5p has been involved in the shikonin-inhibited EMT process via inhibition of Snail and induction of E-cadherin expressions.…”

Section: Dovepressmentioning

confidence: 98%

<p>Regulations of miR-183-5p and Snail-Mediated Shikonin-Reduced Epithelial-Mesenchymal Transition in Cervical Cancer Cells</p>

Tang¹,

Liu²,

Zhang³

et al. 2020

DDDT

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Background: Shikonin, the main ingredient of Lithospermum erythrorhizon, has been reported to have antitumor effects via multiple targets and signaling pathways. However, the detailed mechanism underlying the effects in cervical cancer still remained unknown. Methods: MTT, wound-healing, transwell assays and flow cytometry experiments were used to measure cell growth, migration, invasion, and cell cycle analysis. Western blot was used to examine protein levels of Snail, Vimentin and E-cadherin. The expression level of miR-183-5p was measured via qRT-PCR. The E-cadherin promoter activity was detected via Secrete-PairTM Dual Luminescence Assay Kit. The transient transfection experiments were used for silencing of E-cadherin and overexpression of Snail genes. Tumor xenograft and bioluminescent imaging experiments were carried out to confirm the in vitro findings. Results: We showed that shikonin inhibited cell viability, migration and invasion, and induced cell cycle arrest in a dose-dependent manner in cervical cancer Hela and C33a cells. Mechanistically, we found that shikonin increased miR-183-5p expression and inhibited expression of transcription factor Snail protein. The mimics of miR-183-5p reduced, while the inhibitors of miR-183-5p reversed shikonin-inhibited Snail protein expression. In addition, shikonin decreased Vimentin, increased E-cadherin protein expressions and E-cadherin promoter activity, the latter was reversed in cells transfected with exogenous Snail overexpression vectors. Moreover, silencing of E-cadherin significantly abolished shikonin-inhibited cervical cancer cell growth. Similar findings were also observed in vivo using one xenograft mouse model. Conclusion: Our results show that shikonin inhibits EMT through inhibition of Snail and stimulation of miR-183-5p expressions, which resulted in induction of E-cadherin expression. Thus, blockade of EMT could be a novel mechanism underlying the anti-cervical cancer effects of shikonin.

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Section: Dovepressmentioning

confidence: 98%

<p>Regulations of miR-183-5p and Snail-Mediated Shikonin-Reduced Epithelial-Mesenchymal Transition in Cervical Cancer Cells</p>

Tang¹,

Liu²,

Zhang³

et al. 2020

DDDT

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“…MiR-183 can significantly reduce the expression of ITGB1, thereby inhibiting cell migration and adhesion. MiR-183 is downregulated in cervical cancer cell line HeLa, and miR-183 directly regulates the invasion and metastasis of HeLa cells by acting on its target gene ITGB1 [44].…”

Section: Roles Of Mir-183 In Cell Migration and Invasionmentioning

confidence: 99%

MicroRNA-183 in Cancer Progression

Cao¹,

Di²,

Liang³

et al. 2020

J. Cancer

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MicroRNA -183(miR-183) is abnormally expressed in many kinds of tumors. It participates in the initiation and development of tumors. There are many pathways regulate the expression of miR-183. The action mechanism of miR-183 in cancer is very extensive, and contradictory conclusions are often drawn. It was upregulated in 18 kinds of cancer, downregulated in 6 kinds of cancer. In addition, there are seven types of cancer, both upregulated and downregulated reports can be found. Evidence showed that miR-183 can not only directly play the role of oncogene or antioncogene, but also regulate the expression of other oncogene or antioncogene in different cancer types. In this review, we discuss the regulator of miR-183 and summarized the expression of miR-183 in different cancers. We also counted the target genes of miR-183 and the functional roles they play. Furthermore, we focused on the roles of miR-183 in cell migration, cell invasion, epithelial-mesenchymal transition (EMT) and microangiogenesis, which play the most important roles in cancer processes. It sheds light on the likely reasons why miR-183 plays different roles in various cancers. In addition, miR-183 and its downstream effectors have the potential to be promising prognostic markers and therapeutic targets in cancer.

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“…Here, our data supported the tumor-promoting property of circ_0018289 in cervical cancer. We identified that circ_0018289 bound to miR-183-5p, a potent suppressor in cervical cancer [ 12 , 13 ]. Furthermore, we demonstrated that the circ_0018289/miR-183-5p axis-mediated transmembrane p24 trafficking protein 5 (TMED5) expression impacted cervical carcinogenesis and angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

Identification of a novel circ_0018289/miR-183-5p/TMED5 regulatory network in cervical cancer development

et al. 2021

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Background Circular RNAs (circRNAs) are increasingly implicated in regulating human carcinogenesis. Previous work showed the oncogenic activity of circ_0018289 in cervical cancer. However, the molecular basis underlying the modulation of circ_0018289 in cervical carcinogenesis is still not fully understood. Methods The levels of circ_0018289, microRNA (miR)-183-5p, and transmembrane p24 trafficking protein 5 (TMED5) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Ribonuclease (RNase) R and subcellular localization assays were used to characterize circ_0018289. Cell proliferation was detected by the Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2′-deoxyuridine (Edu) assays. Cell apoptosis and tube formation were assessed by flow cytometry and tube formation assays, respectively. A dual-luciferase reporter assay was performed to confirm the direct relationship between miR-183-5p and circ_0018289 or TMED5. The role of circ_0018289 in tumor growth was gauged by mouse xenograft experiments. Results Circ_0018289 was overexpressed in cervical cancer tissues and cells. Circ_0018289 silencing impeded cell proliferation, enhanced cell apoptosis, and suppressed angiogenesis in vitro, as well as diminished tumor growth in vivo. Mechanistically, circ_0018289 targeted and regulated miR-183-5p by binding to miR-183-5p, and circ_0018289 regulated cervical cancer development and angiogenesis partially through miR-183-5p. Moreover, TMED5 was directly targeted and inhibited by miR-183-5p through the perfect complementary sites in TMED5 3′UTR, and TMED5 knockdown phenocopied miR-183-5p overexpression in suppressing cervical cancer development and angiogenesis. Furthermore, circ_0018289 induced TMED5 expression by competitively binding to shared miR-183-5p. Conclusion Our observations identified the circ_0018289/miR-183-5p/TMED5 regulatory network as a novel molecular basis underlying the modulation of cervical carcinogenesis.

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MicroRNA-183-5p Inhibits Aggressiveness of Cervical Cancer Cells by Targeting Integrin Subunit Beta 1 (ITGB1)

Cited by 20 publications

References 22 publications

<p>Regulations of miR-183-5p and Snail-Mediated Shikonin-Reduced Epithelial-Mesenchymal Transition in Cervical Cancer Cells</p>

<p>Regulations of miR-183-5p and Snail-Mediated Shikonin-Reduced Epithelial-Mesenchymal Transition in Cervical Cancer Cells</p>

MicroRNA-183 in Cancer Progression

Identification of a novel circ_0018289/miR-183-5p/TMED5 regulatory network in cervical cancer development

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