HERG1 functions as an oncogene in pancreatic cancer and is downregulated by miR-96

Jin, Feng; Yu, Junbo; Pan, Xiaolin; Li, Zengliang; Chen, Zheng; Zhang, Wenjie; Wang, Bin; Yang, Li; Xu, Hao; Zhang, Guoxin; Xu, Zekuan

doi:10.18632/oncotarget.2200

Cited by 53 publications

(63 citation statements)

References 47 publications

(45 reference statements)

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“…Notably, the inhibitory effect of miR-96 on pancreatic cancer cell proliferation has been clearly elucidated in the past few years [20, 51, 89, 90]. In pancreatic cancer, three important oncogenes, including KRAS [51], human either a go-go-related gene type 1 (HERG1) [89] and Glypican 1 (GPC1) [90], are known to be miR-96 target genes.…”

Section: Resultsmentioning

confidence: 99%

“…In pancreatic cancer, three important oncogenes, including KRAS [51], human either a go-go-related gene type 1 (HERG1) [89] and Glypican 1 (GPC1) [90], are known to be miR-96 target genes. KRAS, aberrantly activated in approximately 90% of pancreatic cancers [91], can promote abnormal cell proliferation by activating PI3K/Akt, NF-κB and ERK signaling pathways [92–95].…”

Section: Resultsmentioning

confidence: 99%

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Dysregulation and functional roles of miR-183-96-182 cluster in cancer cell proliferation, invasion and metastasis

Liang

Fan

et al. 2016

Oncotarget

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Previous studies have reported aberrant expression of the miR-183-96-182 cluster in a variety of tumors, which indicates its' diagnostic or prognostic value. However, a key characteristic of the miR-183-96-182 cluster is its varied expression levels, and pleomorphic functional roles in different tumors or under different conditions. In most tumor types, the cluster is highly expressed and promotes tumorigenesis, cancer progression and metastasis; yet tumor suppressive effects have also been reported in some tumors. In the present study, we discuss the upstream regulators and the downstream target genes of miR-183-96-182 cluster, and highlight the dysregulation and functional roles of this cluster in various tumor cells. Newer insights summarized in this review will help readers understand the different facets of the miR-183-96-182 cluster in cancer development and progression.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Dysregulation and functional roles of miR-183-96-182 cluster in cancer cell proliferation, invasion and metastasis

Liang

Fan

et al. 2016

Oncotarget

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“…miR-96 functions as an oncomiR by promoting cellular growth, invasiveness and metastasis in breast cancer [104] , pancreatic cancer [105] and HCC [106] . miR-96 directly targets AKT1S1 that encodes for PRAS40, a negative regulator of mTOR kinase, which prevents the binding of mTOR to its substrates [107] .…”

Section: Mirnas That Activate Mtor Pathwaymentioning

confidence: 99%

Emerging Role of MicroRNAs in mTOR Signaling

Zhang

Huang

Wang³

et al. 2017

Cell. Mol. Life Sci.

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Mechanistic target of rapamycin (mTOR) is a conserved serine/threonine kinase that plays a critical role in the control of cellular growth and metabolism. Hyperactivation of mTOR pathway is common in human cancers, driving uncontrolled proliferation. MicroRNA (miRNA) is a class of short noncoding RNAs that regulate the expression of a wide variety of genes. Deregulation of miRNAs is a hallmark of cancer. Recent studies have revealed interplays between miRNAs and the mTOR pathway during cancer development. Such interactions appear to provide a fine-tuning of various cellular functions and contribute qualitatively to the behavior of cancer. Here we provide an overview of current knowledge regarding the reciprocal relationship between miRNAs and mTOR pathway: regulation of mTOR signaling by miRNAs and control of miRNA biogenesis by mTOR. Further research in this area may prove important for the diagnosis and therapy of human cancer.

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“…The results of the current study revealed that HERG1 expression was significantly increased in bladder cancer cell lines compared with that in SV-HUC-1 cells. Bioinformatic analysis has demonstrated that HERG1 may be a target gene of miR-96 (39). The present study also utilized a dual luciferase reporter assay to verify that HERG1 was a target gene of miR-96.…”

Section: Cell Cycle % Apoptosis % ---------------------------------mentioning

confidence: 81%

Anticancer effect of miR-96 inhibitor in bladder cancer cell lines

et al. 2018

Oncol Lett

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Abstract. The present study aimed to investigate the role of microRNA-96 (miR-96) in the proliferation, invasion and apoptosis of bladder cancer cell lines, and the associated mechanisms. The expression of miR-96 and human ether-à-go-go-related (HERG1) potassium channel in the normal uroepithelium SV-HUC-1 cell line, and bladder cancer T24 and 5637 cell lines were examined using reverse transcription-polymerase chain reaction or/and western blotting. Transfection with miR-96 inhibitor or scrambled control (SC) was used to study the biological activities of miR-96 in bladder cancer cell lines. MTT, flow cytometric and Transwell assays were applied to detect cell viability, apoptosis and invasion, respectively. A dual-luciferase reporter assay was applied to determine the association between miR-96 and HERG1 expression. As demonstrated, miR-96 was highly expressed in the two bladder cancer cell lines, particularly in T24 cells. Following transfection with miR-96 inhibitor, miR-96 expression was significantly reduced in the T24 cell line, compared with SC. The miR-96 inhibitor suppressed cell proliferation and invasion, promoted apoptosis and arrested the cell cycle at the G 1 phase. Consistently, HERG1 was also highly expressed in the two bladder cancer cell lines at the mRNA and protein level, but not in the normal uroepithelium cell line. The miR-96 inhibitor also significantly decreased HERG1 expression compared with SC. The results of the dual-luciferase reporter assay indicated that miR-96 directly targeted wild-type HERG1. In conclusion, miR-96 inhibitor exhibited anticancer effects on bladder cancer cells by inhibiting proliferation and invasion of cells, and promoting their apoptosis. HERG1 was an important target of miR-96. These results provided experimental evidence supporting miR-96 as a therapeutic target for patients with bladder cancer.

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HERG1 functions as an oncogene in pancreatic cancer and is downregulated by miR-96

Cited by 53 publications

References 47 publications

Dysregulation and functional roles of miR-183-96-182 cluster in cancer cell proliferation, invasion and metastasis

Dysregulation and functional roles of miR-183-96-182 cluster in cancer cell proliferation, invasion and metastasis

Emerging Role of MicroRNAs in mTOR Signaling

Anticancer effect of miR-96 inhibitor in bladder cancer cell lines

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