MiR-199a-5p and let-7c cooperatively inhibit migration and invasion by targeting MAP4K3 in hepatocellular carcinoma

Liu, Huan; Lu, Liqin; Ai-hong, Zheng; Xie, Jiaxin; Xue, Qingwu; Wang, Fuwei; Wang, Xiao; Zhou, Hongying; Tong, Xiangmin; Li, Yaqing; Zhu, Xiuming; Wu, Guojun

doi:10.18632/oncotarget.14623

Cited by 28 publications

(36 citation statements)

References 35 publications

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“…Furthermore, miR-199a-5p was investigated to play a variety of roles in cancers. Liu et al elucidated miR-199a-5p and let-7c suppressed hepatocellular carcinoma cells metastasis capacity in [18]. In the current research, our purpose was to explore circPVT1 and miR-199a-5p function and mechanism in U591 and U251 cells.…”

Section: Introductionmentioning

confidence: 93%

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

Chi

Yang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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2020) Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-ABSTRACT Background: Glioblastoma multiforme (GBM) is one of the most prevailing primary brain tumours among adults and most aggressive cancers. Despite multiple developments in medical and surgical treatments, GBM is still a deadly disease with a high mortality rate. Here, this study was performed to investigate the function of circPVT1 on GBM. Methods: CCK-8 and flow cytometry were utilised to estimate viability and apoptosis in both cells. qRT-PCR was performed to determine circPVT1 and miR-199a-5p expression. Western blot was conducted to determine apoptosis, migration and EMT-related proteins levels when silencing circPVT1. Subsequently, these parameters were re-tested after up-regulating miR-199a-5p. Results: CircPVT1 was highly expressed in GBM tissues. Silencing circPVT1 raised two cells apoptosis and reduced viability and migration capacity. Moreover, EGF-induced EMT was repressed by silencing circPVT1. In addition, miR-199a-5p expression was elevated when silencing circPVT1. And silencing circPVT1 exerted above changes via up-regulating miR-199a-5p. Finally, silencing circPVT1 repressed YAP1 and PI3K/AKT pathways via up-regulating miR-199a-5p. Conclusion: Our data suggested that silencing circPVT1 inhibited viability, migration, EGF-induced EMT and promoted apoptosis as well as repressed YAP1 and PI3K/AKT pathways by up-regulating miR-199a-5p. HIGHLIGHTS 1. CircPVT1 expression is highly expressed in GBM tissues; 2. Si-circPVT1 represses migration and promoted apoptosis in U539 and U251 cells; 3. Si-circPVT1 represses migration and promoted apoptosis when elevating miR-199a-5p; 4. Si-circPVT1 represses EGF-induced EMT when increasing miR-199a-5p; 5. Si-circPVT1 suppresses YAP1 and PI3K/AKT pathways by up-regulating miR-199-5p. ARTICLE HISTORY

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Section: Introductionmentioning

confidence: 93%

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

Chi

Yang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…MAP4K3 has been previously reported to regulate cell death (11). In hepatocellular carcinoma cell lines, MAP4K3 has also been shown to induce cell migration and invasion (12). Overexpression of MAP4K3 was identified in NSCLC tumor tissues (13), and correlated with recurrence in patients with NSCLC (14).…”

Section: Introductionmentioning

confidence: 97%

MicroRNA‑98‑5p regulates the proliferation and apoptosis of A549�cells by targeting MAP4K3

et al. 2019

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Non-small cell lung cancer (NSCLC) is a primary subtype of lung cancer that is accompanied by a high incidence rate and poor prognosis. The primary treatment for NSCLC is chemotherapy, which has low effectiveness and high toxicity. Thus, novel targeted therapy has drawn much attention in recent years. MicroRNAs (miRs) serve important roles in multiple cancer types. In the current study, a decrease in miR-98-5p and an increase in mitogen-activated protein kinase kinase kinase kinase 3 (MAP4K3) was observed in NSCLC tumor tissues compared with normal tissues. miR-98-5p was predicted to target positions 1,056-1,063 of the MAP4K3 3'-untranslated region (UTR). The binding sites between miR-98-5p and the 3'-UTR of MAP4K3 messenger RNA were supported by the results of a dual-luciferase reporter assay. Compared with the control and miR-negative control (NC) groups, miR-98-5p mimic significantly reduced cell proliferation and increased apoptosis in NSCLC cells. In addition, miR-98-5p mimic reduced the expression of MAP4K3 and mammalian target of rapamycin while increasing the expression of cleaved caspase-3 compared with the control group and miR-NC groups. In conclusion, miR-98-5p may inhibit the progression of NSCLC via targeting of MAP4K3.

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“…MAP4K3 (also known as serine/threonine protein kinase GLK) is a member of MAPK kinase that regulates a variety of cellular activities, including cell proliferation, cell migration, and cell differentiation [20,21]. Upregulation of MAP4K3 is a major factor in the development and progression of various tumors [22][23][24]. MAP4K3 was rstly identi ed to play an ongogenic role in paediatric high grade glioma [25].…”

Section: Discussionmentioning

confidence: 99%

LncRNA SBF2-AS1 Promotes Malignant Phenotypes and Radioresistance of Glioblastoma Cells by Impairing miR-338-3p-targeted MAP4K3 Inhibition

Pan¹,

Xu²,

Wang³

et al. 2020

Preprint

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Background: Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumors in adults. LncRNA SBF2-AS1 has been reported to promote malignant progression in multiple human cancers. However, the roles and underlying mechanisms of SBF2-AS1 in GBM are still unknown.Methods: The levels of SBF-AS1 were identified in GBM tissues and normal brain tissues, and in GBM cell lines and normal human astrocytes. The effect of SBF2-AS1 on proliferation, invasion and radiosensitivity was evaluated by CCK-8 assay, transwell assay, γ-H2AX foci assay and clonogenic survival assay in vitro and in vivo. The interactions among SBF2-AS1, miR-338-3p and MAP4K3 were validated through luciferase report, RNA immunoprecipitation and western blot assays. Results: In the present study, we comfirmed that SBF2-AS1 was highly upregulated in GBM tissues and cell lines, and its levels were markedly higher in WHO stage III-IV gliomas compared with WHO stage I-II gliomas. Kaplan-Meier survival analysis revealed that glioma patients with high SBF2-AS1 expression had shorter overall survival than those with low SBF2-AS1 expression. SBF2-AS1 inhibition suppressed the proliferation of GBM cells by down-reguating of Ki-67 and CyclinD1. Moreover, silencing SBF2-AS1 increased the proportion of cells in G1 phase and decreased the proportion of cells in S phase. In addition, SBF2-AS1 inhibition suppressed the invasion of GBM cells by down-reguating of MMP2 and MMP9. Xenograft tumor models revealed that the silencing of SBF2-AS1 inhibited tumor growth in vivo. Moreover, the silencing of SBF2-AS1 significantly sensitized GBM cells to radiation in vitro and in vivo. Indeed, we observed a persistence of γ-H2AX staining after ionizing radiation, leading to enhanced DNA repair and radioresistance. Mechanistically, SBF2-AS1 inhibition reduced the expression of MAP4K3 by directly binding with miR-338-3p in GBM cells. Conclusions: Our study demonstrated that SBF2-AS1 enhanced cell proliferation, invaison and radioresistance via modulating miR-338-3p/MAP4K3 axis, and it is an attractive therapeutic target to overcome radioresistance of GBM.

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MiR-199a-5p and let-7c cooperatively inhibit migration and invasion by targeting MAP4K3 in hepatocellular carcinoma

Cited by 28 publications

References 35 publications

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

MicroRNA‑98‑5p regulates the proliferation and apoptosis of A549�cells by targeting MAP4K3

LncRNA SBF2-AS1 Promotes Malignant Phenotypes and Radioresistance of Glioblastoma Cells by Impairing miR-338-3p-targeted MAP4K3 Inhibition

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