OCT4B modulates OCT4A expression as ceRNA in tumor cells

Liu, Dong; Yang, Zhengyan; Bu, Jingyi; Xu, Chunyan; Sun, Hui; Tang, Jingling; Lin, Ping; Cheng, Wenli; Huang, Ning; Cui, Rongjun; Yu, Xiuchong; Zheng, Xiaodong

doi:10.3892/or.2015.3862

Cited by 33 publications

(23 citation statements)

References 51 publications

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“…However, the ratio of OCT4A to OCT4B was observed to vary among different cell lines. This could be an important factor for cancer cell biology, since the two variants may influence one another's function; the data provided in the present manuscript supports this claim, as does recent work from other groups (33).…”

Section: Discussionsupporting

confidence: 88%

OCT4B regulates p53 and p16 pathway genes to prevent apoptosis of breast cancer cells

Meng

Zhi

et al. 2018

Oncol Lett

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Octamer-binding transcription factor 4 (OCT4) is a transcription factor with a well-defined role in stem cell pluripotency. Two OCT4 isoforms, OCT4A and OCT4B, tend to be downregulated as normal cells differentiate. However, OCT4, particularly OCT4B, may become reactivated in cancer cells. Despite this observation, the exact function of OCT4B re-expression in cancer is unclear. In the present study, the role of OCT4 in breast cancer cells was determined. In particular, the ability of OCT4 to regulate key genes involved in cellular proliferation and apoptosis, two pathways that are frequently deregulated in cancer, was examined. The cyclin-dependent kinase inhibitor 2A locus encodes p16INK4a and p14ARF, two important cell cycle inhibitors. The tumor suppressor p53 also has well characterized roles in suppressing proliferation and promoting apoptosis. The present study demonstrated, via overexpression and genetic knockdown techniques, that OCT4B regulates the expression of several of these genes and ultimately regulates the rate of apoptosis of MCF-7 breast cancer cells. It was also observed that, while OCT4B and OCT4A regulate one another, it is OCT4B that serves a more prominent role in regulating the transcription of downstream genes. Taken together, the present results suggest that OCT4B is re-expressed in a number of breast cancer cell lines, where it affects both the transcription of cell cycle genes and the rate of apoptosis. These properties of OCT4B may depend on, at least in part, the co-function of OCT4A.

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Section: Discussionsupporting

confidence: 88%

OCT4B regulates p53 and p16 pathway genes to prevent apoptosis of breast cancer cells

Meng

Zhi

et al. 2018

Oncol Lett

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“…The OCT4 gene has three mRNA isoforms: OCT4A, OCT4B, and OCT4B1. Zheng et al reported that OCT4B functioned as a ceRNA to regulate OCT4A expression in an miRNA-dependent manner in several tumor cell lines [ 45 ]. This is the first report showing spliced gene isoforms serving as ceRNAs.…”

Section: Validated Cernas In Human Cancermentioning

confidence: 99%

Competing endogenous RNA networks in human cancer: hypothesis, validation, and perspectives

et al. 2016

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Non-coding RNAs represent a majority of the human transcriptome. However, less is known about the functions and regulatory mechanisms of most non-coding species. Moreover, little is known about the potential non-coding functions of coding RNAs. The competing endogenous RNAs (ceRNAs) hypothesis is proposed recently. This hypothesis describes potential communication networks among all transcript RNA species mediated by miRNAs and miRNA-recognizing elements (MREs) within RNA transcripts. Here we review the evolution of the ceRNA hypothesis, summarize the validation experiments and discusses the significance and perspectives of this hypothesis in human cancer.

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“…Though Oct4b differ in their ability to confer self‐renewal as Oct4a (Guo et al, ; Lee et al, ), it may play a role in epithelial‐to‐mesenchymal transition (Papamichos, Lambropoulos, & Kotoula, ). Recent report showed that Oct4b modulated Oct4a expression as competing endogenous RNA (ceRNA) in tumor cells (Li, Yang, et al, ). Human OCT4B1 had a positive correlation with pluripotency (Atlasi et al, ; Papamichos et al, ).…”

Section: Introductionmentioning

confidence: 99%

Characterization of novel alternative splicing variants of Oct4 gene expressed in mouse pluripotent stem cells

Liu

Sun

et al. 2018

Journal Cellular Physiology

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Oct4 is an important transcription factor for maintaining self-renewal and pluripotency of pluripotent stem cells (PSCs). Human OCT4 can be alternatively spliced and generate OCT4a, OCT4b, and OCT4b1. In this study, we discovered the novel Oct4 variants of Oct4b' and Oct4b1-3 in mouse PSCs for the first time. The expression of Oct4b variants, especially for Oct4b', was down regulated along with the downregulation of Oct4a when stem cells were differentiated. We also found four Oct4 translational products that were differentially expressed in mouse PSCs under the different culture conditions. The constructs of Oct4b2 and Oct4b3 could be alternatively spliced into Oct4b and Oct4b' when constructs were transiently transfected in NIH3T3 cells. Oct4b' encoded a 189 aa protein, and Oct4b could generate three distinct proteins including Oct4b-246aa, Oct4b-221aa, and Oct4b-189aa. The Oct4b variants could be alternatively translated in different type cells under the control of internal ribosome entry site (IRES) element that is within 5' upstream sequence of Oct4b. These findings provide new insights into reconsidering Oct4 variants expression and its additional role in maintaining the pluripotency of stem cells.

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OCT4B modulates OCT4A expression as ceRNA in tumor cells

Cited by 33 publications

References 51 publications

OCT4B regulates p53 and p16 pathway genes to prevent apoptosis of breast cancer cells

OCT4B regulates p53 and p16 pathway genes to prevent apoptosis of breast cancer cells

Competing endogenous RNA networks in human cancer: hypothesis, validation, and perspectives

Characterization of novel alternative splicing variants of Oct4 gene expressed in mouse pluripotent stem cells

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