MicroRNA-15a Inhibits Proliferation and Induces Apoptosis in CNE1 Nasopharyngeal Carcinoma Cells

Zhu, Kangshun; He, Ying; Cui, Xia; Yan, Jun; Hou, Jin; Kong, Demin; Yang, Yilin; Zheng, Guoxi

doi:10.3727/096504016x14611963142290

Cited by 26 publications

(17 citation statements)

References 29 publications

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“…Moreover, many miRs have been reported to direct target oncogenes or tumor suppressors, and thus play suppressive or promoting roles in human cancers (10,12–14). In recent decade, deregulations of specific miRs have been implicated in NPC development and progression, such as miR-15a, miR-138, miR-214, miR-218, and miR-663b (15–19). Yi et al reported that inhibition of miR-663 suppressed the proliferation of NPC CNE1 and 5-8F cells in vitro , and the NPC tumor growth of xenografts in nude mice (19).…”

Section: Introductionmentioning

confidence: 99%

miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2

Liang

Zhang

Deng

et al. 2017

Experimental and Therapeutic Medicine

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The authors' previous study revealed that the serum levels of microRNA (miR)-663b are significantly increased in patients with nasopharyngeal carcinoma (NPC), and are associated with NPC progression and poor prognosis. However, the molecular mechanism of underlying NPC growth and metastasis remains unclear. In the present study, quantitative polymerase chain reaction and western blot analyses were performed to examine changes to mRNA and protein expression, respectively. MTT, wound healing and Transwell assays were used to examine cell proliferation, migration and invasion, respectively. Luciferase reporter gene assays were performed to identify target genes of miR-663b. It was demonstrated that miR-663b was significantly upregulated in NPC tissue compared with non-tumor nasopharyngeal epithelial tissue samples. Furthermore, miR-663b expression gradually increased with advancing stages of NPC, with the highest expression being observed in the latest stage IV. The increased expression of miR-663b was associated with advanced clinical stage and lymph node metastasis. In addition, miR-663b expression was increased in NPC cell lines compared with normal nasopharyngeal epithelial NP69 cells. Knockdown of miR-663b resulted in a significant reduction in the proliferation, migration and invasion of NPC CNE1 cells. Tumor suppressor candidate 2 (TUSC2) was identified as a novel target gene of miR-663b. It was further demonstrated that TUSC2 was significantly downregulated in NPC tissue samples and cell lines. miR-663b negatively regulated the expression of TUSC2 at the post-transcriptional level in CNE1 cells. Additionally, inhibition of TUSC2 expression attenuated the suppressive effects of miR-663b downregulation on the proliferation, migration and invasion of CNE1 cells. To the best of our knowledge, this is the first study to demonstrate that miR-663b, which is upregulated in NPC, promotes the proliferation, migration and invasion of NPC cells, partially through the inhibition of TUSC2 expression. Therefore, it is suggested that miR-663b is a promising therapeutic target for the treatment of patients with NPC.

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Section: Introductionmentioning

confidence: 99%

miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2

Liang

Zhang

Deng

et al. 2017

Experimental and Therapeutic Medicine

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“…For example, abnormal overexpression of miR-15a-5p was reported to suppress cancer proliferation, induce cell cycle arrest in human HCC cells, and have a specific and negative regulating effect on BDNF (6). In addition, the protein levels of p27, GSK-3beta, Bax, procaspase3, and active caspase 3 were upregulated by the overexpression of miR-15a, which inhibited proliferation and induced apoptosis of CNE1 cells (10). There were other studies that investigated the role of miR-15a in OA.…”

Section: Discussionmentioning

confidence: 99%

MiR-15a-5p regulates viability and matrix degradation of human osteoarthritis chondrocytes <i>via</i> targeting VEGFA

Chen

Tian

2016

BST

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“…MicroRNAs (miRs), a class of small non-coding RNAs, can directly bind to the 3' untranslated region (UTR) of their target mRNAs, and cause RNA degradation or translation inhibition (7,8). Through mediating the expression of their target genes, miRs are involved in various cellular biological processes, including cell proliferation, differentiation, migration and invasion, as well as tumorigenesis (9)(10)(11). A large number of miRs have been demonstrated to have promoting or suppressive roles in various human cancer types, including cervical cancer, and certain miRs are strongly associated with HPV (12,13).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑130a regulated by HPV18 E6 promotes proliferation and invasion of cervical cancer cells by targeting TIMP2

et al. 2019

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Human papillomaviruses (HPVs) have important roles in the development and progression of cervical cancer, but the underlying mechanisms are yet to be fully elucidated. MicroRNA-130a (miR-130a) has previously been reported to promote cervical cancer growth. However, the underlying molecular mechanisms by which miR-130a promotes cervical cancer progression have remained largely elusive. In the present study, polymerase chain reaction and western blot analyses were performed to examine the expression levels of miR-130a and associated proteins. A wound healing assay and a Transwell assay were applied to study cell migration and invasion. A luciferase reporter gene assay was performed to confirm the targeting associations of miR-130a. It was observed that miR-130a was significantly upregulated in cervical cancer tissues compared with that in adjacent non-tumorous tissues. High expression of miR-130a was significantly associated with lymph node metastasis and an advanced clinical stage of cervical cancer. Furthermore, the expression of miR-130a was also higher in HPV(+) cervical cancer cell lines compared with that in HPV(-) cells. Knockdown of HPV18 E6 significantly inhibited the expression of miR-130a in HeLa cervical cancer cells. Furthermore, knockdown of miR-130a reduced the migration and invasion of HeLa cells. Tissue inhibitor of metalloproteinase 2 (TIMP2), an antagonist of matrix metalloproteinase 2 (MMP2), was identified as a novel, direct target gene of miR-130a. The expression of TIMP2 was negatively mediated by miR-130a, and HPV18 E6 inhibited the expression of TIMP2 in HeLa cells. Furthermore, knockdown of TIMP2 rescued the suppressive effects of miR-130a downregulation on the migration and invasion of HeLa cells. In summary, the present study suggests that HPV18 E6 promotes the expression of miR-130a, which further inhibits the expression of TIMP2 and promotes cervical cancer cell invasion. Therefore, HPV/miR-130a/TIMP2 signaling may be a potential target for the prevention of cervical cancer metastasis.

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MicroRNA-15a Inhibits Proliferation and Induces Apoptosis in CNE1 Nasopharyngeal Carcinoma Cells

Cited by 26 publications

References 29 publications

miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2

miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2

MiR-15a-5p regulates viability and matrix degradation of human osteoarthritis chondrocytes <i>via</i> targeting VEGFA

MicroRNA‑130a regulated by HPV18 E6 promotes proliferation and invasion of cervical cancer cells by targeting TIMP2

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