MicroRNA-326 suppresses the proliferation, migration and invasion of cervical cancer cells by targeting ELK1

Zhang, Ping; Kong, Feng; Deng, Xinchao; Yu, Yunhai; Hou, Chunying; Liang, Tingting; Zhu, Lin

doi:10.3892/ol.2017.5852

Cited by 43 publications

(33 citation statements)

References 36 publications

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“…Moreover, miR-326 overexpression could also suppress tumorigenesis in vivo. Consistent with the existing studies, miR-326 could have an abnormal expression in various human cancers and negatively regulate the procession of tumors [33][34][35]. These findings can offer supporting evidence for the suppressive roles of miR-326 in PTC.…”

Section: Discussionsupporting

confidence: 88%

miR-326 inhibits the progression of papillary thyroid carcinoma by targeting MAPK1 and ERBB4

Nie

Wei

et al. 2020

neo

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Papillary thyroid carcinoma (PTC) is the prevalent histotype of thyroid cancer, with increasing incidence worldwide. MicroRNAs (miRNAs) could play an important role in the development and progression of human cancers. Interestingly, miR-326 was validated as one of the downregulated miRNAs in PTC. Therefore, it is necessary to research the function of miR-326 involved in the progression of PTC. In the current study, we detected the downregulation of miR-326 in PTC tissues and cell lines. The miR-326 overexpression or knockdown was conducted in TPC-1 or HTh83 PTC cells. miR-326 mimics decreased the proliferation, clone formation ability and caused G1-phase accumulation. In addition, the reduction of migration and invasion abilities was induced by miR-326 mimics. Western blot analysis showed that the cells with miR-326 mimics exhibited the inhibition of vimentin and N-cadherin, as well as enhancement of E-cadherin. Importantly, miR-326 could directly target mitogen activated protein kinase 1 (MAPK1) and epidermal growth factor receptor 4 (ERBB4). MAPK1 or ERBB4 overexpression rescued the effects of miR-326 on proliferation, migration, and invasion in PTC cells. Notably, miR-326 reduced tumorigenesis in vivo, including the decrease of tumor volume and weight, suppression of Ki-67, N-cadherin, MAPK1 and ERBB4. In all, these results might provide a new therapeutic target for the diagnosis of PTC.

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Section: Discussionsupporting

confidence: 88%

miR-326 inhibits the progression of papillary thyroid carcinoma by targeting MAPK1 and ERBB4

Nie

Wei

et al. 2020

neo

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“…Previous studies have demonstrated that miRNAs are a novel class of regulatory molecules in various human cancers (39,40). The abnormal expression of miRNAs is closely related to malignant biological behaviour, which include proliferation, invasion, apoptosis, cell cycle and angiogenesis (41)(42)(43). Therefore, miRNAs may be investigated as a novel candidate and screening tool in the clinical diagnosis, therapy and prognosis of GBM.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-485 inhibits malignant biological behaviour of glioblastoma cells by directly targeting PAK4

Mao

Lei

Zhang

et al. 2017

International Journal of Oncology

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Glioblastoma (GBM), which is characterised by rapid growth, cellular heterogeneity, angiogenesis, extensive invasion, hypoxia and necrosis, is the most common histological subtype of glioma in adults. MicroRNA (miRNA) dysregulation is a common feature of human cancers, including GBM. Previous studies have suggested that miRNAs are a novel class of regulatory molecules in various human cancers. Therefore, miRNAs may be investigated as a novel candidate and screening tool in the clinical diagnosis, therapy and prognosis of GBM. Recent accumulating evidence has demonstrated that miRNA‑485 (miR‑485) is involved in the development and progression of several types of human cancers. However, the expression level, exact role and underlying mechanisms of miR‑485 in GBM remain unclear. In this study, miR‑485 was downregulated in both GBM tissue specimens and cell lines. miR‑485 overexpression inhibited GBM cell proliferation, colony formation, migration and invasion; increased apoptosis in vitro; and reduced tumour growth in vivo. In addition, p21‑activated kinase 4 (PAK4) was demonstrated to be a direct and functional target of miR‑485 in GBM. Furthermore, PAK4 was upregulated in GBM tissues and negatively correlated with miR‑485 expression. Moreover, PAK4 knockdown exhibited a similar effect to miR‑485 overexpression in GBM cells. Enforced expression of PAK4 rescued miR‑485 tumour‑suppressor functions in GBM cells. miR‑485 inhibited the activation of the AKT and ERK signalling pathways in GBM. These results indicate that miR‑485 acts as a tumour suppressor in GBM by, at least partially, directly targeting PAK4 and regulating the AKT and ERK signalling pathways. Thus, miR‑485 may be a potential target for the treatment of patients with GBM.

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“…miRNAs may serve as either tumour suppressors or oncogenes in different types of human malignancies, and this mainly depends on the functional characteristics of their target genes (19). Lowly expressed miRNAs may normally play tumour-suppressing roles through the regulation of oncogenes (20), whereas upregulated miRNAs may act as oncogenes during tumour initiation and progression by repressing tumour-suppressor genes (21). Therefore, investigation of cancer-related miRNAs may identify novel therapeutic targets for anti-tumour therapy.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

Liu

et al. 2018

Oncol Rep

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Retinoblastoma (RB) is the most common primary intraocular malignancy during infancy and childhood worldwide. Numerous microRNAs (miRNAs) contribute to RB initiation and progression through the regulation of cell proliferation, cycle, apoptosis, migration, invasion and metastasis. Therefore, further investigation concerning the expression, roles and associated mechanisms of RB‑related miRNAs may be beneficial to develop novel strategies for patients with this malignancy. Recently, miRNA‑448 (miR‑448) has been reported to be aberrantly expressed and to play an important role in several types of human cancer. However, the expression patterns and biological roles of miR‑448 in RB have not been studied. The aim of the present study was to detect the expression levels of miR‑448 and investigate its functions in RB and its associated molecular mechanisms. In the present study, miR‑448 was significantly downregulated in RB tissues and cell lines. Upregulation of miR‑448 decreased cell proliferation and invasion and increased apoptosis in RB cells. Additionally, ρ‑associated coiled‑coil containing protein kinase 1 (ROCK1) was validated as a novel direct target gene of miR‑448 in RB. ROCK1 was overexpressed in RB tissues and inversely correlated with miR‑448 expression. Furthermore, ROCK1 silencing induced effects on the proliferation, invasion and apoptosis of RB cells similar to those observed following miR‑448 overexpression. Moreover, restoration of miR‑448 expression markedly reversed the effects of miR‑448 overexpression on RB cells, further supporting the hypothesis that ROCK1 is a direct functional target of miR‑448 in RB. Importantly, miR‑448 targeted ROCK1 to inhibit the activation of the PI3K/AKT signalling pathway in RB. These results demonstrated that miR‑448 may serve as a tumour suppressor in RB by directly targeting ROCK1 and regulating the PI3K/AKT signalling pathway, thereby suggesting that miR‑448 may be an effective therapeutic target for treating this aggressive cancer.

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MicroRNA-326 suppresses the proliferation, migration and invasion of cervical cancer cells by targeting ELK1

Cited by 43 publications

References 36 publications

miR-326 inhibits the progression of papillary thyroid carcinoma by targeting MAPK1 and ERBB4

miR-326 inhibits the progression of papillary thyroid carcinoma by targeting MAPK1 and ERBB4

MicroRNA-485 inhibits malignant biological behaviour of glioblastoma cells by directly targeting PAK4

MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

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