Upregulated in Hepatitis B virus-associated hepatocellular carcinoma cells, miR-331-3p promotes proliferation of hepatocellular carcinoma cells by targeting ING5

Cao, Yiyi; Chen, Juan; Wang, Dan; Peng, Hong; Tan, Xixi; Xiong, Dongmei; Huang, Aiping; Tang, Hua

doi:10.18632/oncotarget.5642

Cited by 51 publications

(37 citation statements)

References 39 publications

(42 reference statements)

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“…The proteins of the Inhibitor of Growth (ING) candidate tumor suppressor family include ING1-ING5, which share a highly conserved carboxy-terminal plant homeodomain (PHD) and are involved in multiple cellular functions such as cell cycle regulation, senescence, apoptosis, chromatin remodeling and regulation of autophagy and differentiation [ 1 – 4 ]. ING5 has been identified to physically interact with p300 and p53, and overexpression of ING5 induces apoptosis in colorectal cancer cells [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

ING5 knockdown enhances migration and invasion of lung cancer cells by inducing EMT via EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways

Liu

Zhang

et al. 2017

Oncotarget

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ING5 belongs to the Inhibitor of Growth (ING) candidate tumor suppressor family, whose functions have been involved in the regulation of chromatin remodeling, cell cycle progression, proliferation and apoptosis. Our previous study has shown that ING5 overexpression inhibits lung cancer aggressiveness via suppressing epithelial to mesenchymal transition (EMT). However, the mechanisms remain largely unknown. In the current study, by Phospho-Kinase array and western blot, we have defined significantly upregulated EGFR/PI3K/Akt and IL-6/STAT3 oncogenic signaling pathways in ING5 knockdown A549 cells, which could be downregulated by ING5 overexpression. PI3K inhibitor ZSTK474 or STAT3 inhibitor Niclosamide not only abolished ING5 knockdown-promoted proliferation, colony formation, migration and invasion of lung cancer A549 cells, but also impaired ING5 knockdown-stimulated metastasis of cancer cells in mouse xenograft models with tail vein injection of A549 cells. Furthermore, treatment with ZSTK474 or Niclosamide decreased protein level of EGFR, p-Akt, IL-6 and p-STAT3, and reversed ING5 knockdown-promoted EMT, as indicated by downregulated expression of EMT marker E-cadherin, an epithelial marker, increased expression of N-cadherin, a mesenchymal marker, and EMT-related transcription factors including Snail, Slug, Smad3 and Twist. Taken together, these results demonstrate that loss of ING5 enhances aggressiveness of lung cancer cells by promoting EMT via activation of EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways.

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Section: Introductionmentioning

confidence: 99%

ING5 knockdown enhances migration and invasion of lung cancer cells by inducing EMT via EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways

Liu

Zhang

et al. 2017

Oncotarget

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“…The results in previous study suggest that microRNA-602 plays an important regulatory role in HBx-mediated hepatocarcinogenesis by inhibiting the tumor suppressive function of RASSF1A, from very early stage of chronic HBV hepatitis and HBV-positive cirrhosis through HCC (61). A similar mechanism also exists in miR-331-3p which is upregulated by HBx via enhancing its promoter activity, and miR-331-3p promotes proliferation of HCC cells through targeting ING5 (56). In patients with HCC, miR-216b, which could be reduced by HBx, functions as a tumor suppressor by targeting IGF2BP2 and subsequently suppressing the downstream IGF2, AKT/mTOR and MAPK/ ERK signaling pathways, finally, inducing the proliferation (28).…”

Section: The Influence Of Hbx Through Regulating Mirna For Hepatocarcmentioning

confidence: 85%

The function of miRNAs in hepatocarcinogenesis induced by hepatitis B virus X protein

Wang

Huang

2017

Oncology Reports

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MicroRNAs are short RNAs that play a crucial role in all biological processes through post-transcriptional regulation for protein-coding genes and inducing mRNA degradation. Hepatitis B virus infection has been considered as a major risk factor in hepatocellular carcinoma, further research indicates that hepatitis B virus X protein (HBx) is one of the critical links of hepatocarcinogenesis. HBx takes part in hepatocarcinogenesis via regulating transcription, signal transduction, apoptosis, protein degradation and DNA repair. miRNA is the important target gene of HBx, their interaction impacts many tumor processes, such as proliferation, apoptosis, invasion, metastasis, differentiation and adipogenesis. In the present study we reviewed the current state of knowledge of regulation pathway of HBx acting on miRNAs, and focused on the role of their interplay in hepatocarcinogenesis.

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“…For miR-331, it has been demonstrated to be overexpressed in breast cancer, but its role in breast cancer is unclear [11]. Previously, miR-331 has been linked to the proliferation of hepatocellular carcinoma cells [30]. miR-331 has also been reported to be a tumor suppressor in glioblastoma, which inhibited cell proliferation and clonogenic growth [31].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR-331 Indicates Poor Prognosis and Promotes Progression of Breast Cancer

et al. 2020

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Background: With the increasing number of cases of breast cancer every year, the exploration of novel biomarkers has drawn attention. miR-331 has been demonstrated to play a role in various cancers, but its role in breast cancer is still unknown. Methods: In this study, we included 121 patients with breast cancer treated at Affiliated Hospital of Weifang Medical University. Breast cancer tissues and adjacent normal tissues were collected during the surgery. The expression of miR-331 in breast cancer tissues and cell lines was detected by qRT-PCR assay. Then, with the help of Kaplan-Meier survival and Cox regression analyses, the role of miR-331 in the prognosis of breast cancer was analyzed. Finally, the effect of miR-331 on cell proliferation, migration, and invasion was investigated with CCK-8 assay and transwell assay. Results: miR-331 was significantly upregulated in breast cancer tissues compared with normal tissues. The overexpression of miR-331 was associated with lymph node metastasis, TNM stage, and poor prognosis. From the results of Cox regression analyses, it was found that miR-331 served as an independent indicator in the prognosis of breast cancer. In addition, miR-331 was also found to be upregulated in breast cancer cells, which promoted cell proliferation, migration, and invasion of breast cancer. Conclusion: As shown from our data, miR-331 may be a potential prognostic biomarker in breast cancer. Moreover, the development and progression of breast cancer may involve miR-331. These findings suggest a novel therapeutic target for the treatment of breast cancer.

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Upregulated in Hepatitis B virus-associated hepatocellular carcinoma cells, miR-331-3p promotes proliferation of hepatocellular carcinoma cells by targeting ING5

Cited by 51 publications

References 39 publications

ING5 knockdown enhances migration and invasion of lung cancer cells by inducing EMT via EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways

ING5 knockdown enhances migration and invasion of lung cancer cells by inducing EMT via EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways

The function of miRNAs in hepatocarcinogenesis induced by hepatitis B virus X protein

Overexpression of miR-331 Indicates Poor Prognosis and Promotes Progression of Breast Cancer

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