miR-143 is associated with proliferation and apoptosis involving ERK5 in HeLa cells

Fang, Zheng; Zhang, Jiahe; Luo, Santu; Yi, Jing; Wang, Ping; Zheng, Quan-Qing; Wen, Yurong

doi:10.3892/ol.2016.5016

Cited by 17 publications

(14 citation statements)

References 41 publications

(47 reference statements)

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“…A large body of evidence indicates that miRNAs have an essential role in the development and progression of cervical cancer (30)(31)(32). Thus, miRNAs with dysregulated expression in cervical cancer are potential biomarkers for the diagnosis and prognosis of this disease.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑485 targets MACC1 and inhibits cervical cancer cell proliferation and invasion

et al. 2018

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A large body of evidence has indicated that microRNAs (miRNAs/miRs) have essential roles in the development and progression of cervical cancer. Thus, miRNAs with dysregulated expression are potential biomarkers for cervical cancer diagnosis and prognosis. In the present study, expression levels of miR‑485 were detected in cervical cancer tissues and cell lines. The effects of miR‑485 overexpression on the proliferation and invasion of cervical cancer cells were determined with Cell Counting kit‑8 and Transwell invasion assays. The mechanisms underlying the action of miR‑485 in cervical cancer were investigated using bioinformatics analysis, a luciferase reporter assay, reverse transcription‑quantitative polymerase chain reaction and western blot analysis. In addition, the association between miR‑485 and metastasis associated in colon cancer‑1 (MACC1) in cervical cancer tissues was examined. The present study demonstrated that miR‑485 expression was significantly downregulated in cervical cancer tissues and cell lines. Reduced miR‑485 expression in patients with cervical cancer was correlated with International Federation of Gynecology and Obstetrics stage and lymph node metastasis. Furthermore, restored expression of miR‑485 significantly reduced cervical cancer cell proliferation and invasion. MACC1 was identified as a direct target gene of miR‑485 in cervical cancer. MACC1 expression was significantly upregulated in cervical cancer specimens and was inversely correlated with miR‑485 expression. Additionally, the restored expression of MACC1 eliminated the suppressive effects of miR‑485 overexpression on the proliferation and invasion of cervical cancer cells. Notably, the upregulation of miR‑485 suppressed the MET proto‑oncogene, receptor tyrosine kinase (Met)/RAC‑α serine/threonine‑protein kinase (AKT) signaling pathway. These results demonstrated that miR‑485 may perform its tumor suppressive function in cervical cancer by directly targeting MACC1 and inhibiting the Met/AKT signaling pathway. Therefore, the miR‑485/MACC1 axis may be a novel and effective therapeutic target in cervical cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑485 targets MACC1 and inhibits cervical cancer cell proliferation and invasion

et al. 2018

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“…In addition, Xu’s group demonstrated that the MIR143 overexpression inhibits the cell growth of nasopharyngeal cancer both in vitro and in vivo 58 . Zheng et al demonstrated that the overexpression of MIR143 suppressed the cell proliferation of cervical cancer cells in vitro 59 . They found that MIR143‐3p negatively regulated ERK5 expression, which led to the suppression of cervical cancer cell lines.…”

Section: The Role Of Mir143‐3p On Rat Sarcoma Signaling Network In Vmentioning

confidence: 99%

Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview

et al. 2020

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This is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. AbstractRat sarcoma (RAS) is a well-known oncogene that plays important roles in cancer proliferation, cell survival and cell invasion. RAS exists as three major isoforms, Kirsten rat sarcoma (KRAS), Harvey rat sarcoma (HRAS) and neuroblastoma rat sarcoma (NRAS). Mutations of these genes account for approximately 30% of all cancers.Among them, KRAS mutations are the most common, responsible for 85%, followed by NRAS (12%) and HRAS (3%). Although the development of RAS inhibitors has been explored for over the past decade, so far, no effective inhibitor has been found.MicroRNA (miRNA) are a class of small non-coding RNA that control the gene expression of pleural target genes at the post-transcriptional level. MiRNA play critical roles in the physiological and pathological processes at work in cancers, such as cell proliferation, cell death, cell invasion and metastasis. MicroRNA-143 (MIR143) is known to function as a tumor suppressor in a variety of cancers. One of its known mechanisms is suppression of RAS expression and its effector signaling pathways, such as PI3K/AKT and MAPK/ERK. Within the last five years, we developed a potent chemically modified MIR143-3p that enabled us to elucidate the details of the KRAS signaling networks at play in colon and other cancer cells. In this review, we will discuss the role of MIR143-3p in those RAS signaling networks that are related to various biological processes of cancer cells. In addition, we will discuss the possibility of the use of MIR143 as a therapeutic drug for targeting RAS signaling networks. K E Y W O R D S AKT, ERK, KRAS positive circuit, MAPK, MIR143, PI3K, RAS | 1077 TOKUMARU eT Al.

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“…miR-25-3p was reported to target Sema4C in CC cells thereby regulating the epithelial-mesenchymal transition ( 1 ). miR-143 was determined to be negatively associated with CC cell proliferation and apoptosis ( 13 ). miR-217 was demonstrated to be aberrantly expressed in a number of tumor types, including pancreatic adenocarcinoma and osteosarcoma ( 14 , 15 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑217 functions as a tumor suppressor in cervical cancer cells through targeting Rho‑associated protein kinase 1

Dong

Wang

et al. 2018

Oncol Lett

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The abnormal expression of microRNAs (miRNAs/miRs) has been widely reported in various tumor types. miR-217 was demonstrated to be aberrantly expressed in a number of tumors, including pancreatic adenocarcinoma and osteosarcoma; however, its specific expression pattern has never been investigated in cervical cancer cells. Compared with normal control, the level of Rho-associated protein kinase 1 (ROCK1) expression was markedly increased in cervical cancer tissues and cells compared with that in non-cancerous tissues and cells. The expression of miR-217 was significantly reduced in cervical cancer tissues and cell lines. Overexpression of miR-217 could suppress colony formation and the cell invasion capacity of SiHa and HeLa cells. Flow cytometry indicated that miR-217 significantly increased cell apoptosis in SiHa and HeLa cells. Dual-luciferase reporter assays demonstrated that ROCK1 was a target gene of miR-217. In addition, overexpression of ROCK1 also led to an increased invasion capacity in SiHa cells, even when miR-217 was inhibited, indicating that the anti-invasive effects of miR-217 were mediated through ROCK1. In summary, the results of the present study indicated that miR-217 functions as a tumor suppressor in cervical cancer cells, primarily by targeting ROCK1.

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miR-143 is associated with proliferation and apoptosis involving ERK5 in HeLa cells

Cited by 17 publications

References 41 publications

MicroRNA‑485 targets MACC1 and inhibits cervical cancer cell proliferation and invasion

MicroRNA‑485 targets MACC1 and inhibits cervical cancer cell proliferation and invasion

Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview

MicroRNA‑217 functions as a tumor suppressor in cervical cancer cells through targeting Rho‑associated protein kinase 1

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