Circular RNA circ SET domain containing 2 (circSETD2) inhibits hepatocellular carcinoma cell proliferation and invasion <i>in vivo</i> and <i>in vitro</i>

Sun, Keyan; Zhang, Lei; Chen, Peng; Qi, Debin; Líu, Hao; Bao, Haili; Wang, Xiongwei; Li, Tao

doi:10.1080/21655979.2022.2048577

Cited by 3 publications

(4 citation statements)

References 25 publications

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“…Despite SETD2 mutation rate in HCC patients was only ~ 5%, the abnormality of SETD2 in liver was associated with the occurrence of spontaneous HCC and the progress of HCC induced by DEN and highfat diet in vivo, animal experiments revealed that SETD2 repressed HCC tumorigenesis through maintaining lipid homeostasis and SETD2 de ciency caused abnormal expression of cholesterol metabolic genes and lipid accumulation, the increased lipids activated c-Jun, then inhibited p53 activation and induced HCC. 14 However, the bioinformatic analysis of 374 LIHC patients from TCGA database (Fig. 1) indicated that SETD2 was upregulated in human HCC and high SETD2 expression is related to poor prognosis of HCC, and the expression of SETD2 in HCC patients and HCC cell lines (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…7,[10][11][12] Previous studies have identi ed that SETD2 and its relevant H3K36me3 are closely correlated with the development and progression of hepatocellular carcinoma, but there are different ideas about whether SETD2 and H3K36me3 promote or inhibit hepatocellular carcinoma. [13][14][15] Furthermore, the underlying mechanism of SETD2 in the development and progression of hepatocellular carcinoma is largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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Deficiency of histone H3K36 methyltransferase SETD2 inhibits proliferation and migration of hepatocellular carcinoma through ERK pathway

Yang,

Zhang,

Munyurangabo

et al. 2023

Preprint

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Background Hepatocellular carcinoma (HCC) is one of the leading cause of cancer-related death worldwide. SETD2, as the only known methyltransferase for catalyzing trimethylation of histone H3 lysine 36 (H3K36), has been reported to be associated with several cancers. However, the function of SETD2 in HCC is ambiguous. This work aims to research the function and mechanism of SETD2 in HCC based on bioinformation analysis and cell experiments. Methods SETD2 expression and its relationship with prognosis in LIHC patients were evaluated based on the Cancer Genome Atlas (TCGA) database, the effect of SETD2 silencing and overexpression on HCC cell lines was explored according to CCK-8 assay, colony formation assay and wound healing assay. RNA-seq analysis, western blot and chromatin immunoprecipitation (ChIP) assay were used to explore the potential mechanism of SETD2 in HCC. Results The results indicated that SETD2 expression was upregulated and high SETD2 expression was related to poor prognosis in HCC. SETD2 silencing inhibited the proliferation and migration, and SETD2 overexpression promoted the proliferation and migration in HCC cells. RNA-seq data revealed that differentially expressed genes were dramatically enriched in fibroblast growth factor receptor signaling pathway. FGFBP1, as a FGF-binding protein, ranked in the top 10 among the DEGs. The expression of FGFBP1 in SETD2 silencing BEL-7402 cells was significantly decreased. As the downstream effector of FGFR, ERK phosphorylation level had positive correlation with SETD2. Besides, H3K36me3 directly bound to the promoter of FGFBP1 confirmed by ChIP-qPCR. Conclusions Our findings highlight the promotion role of SETD2/H3K36me3 in HCC proliferation and migration via FGFR-ERK signal pathway. Our studies will advance our understanding of epigenetic dysregulation at HCC progression and provide a rationale for SETD2 as potential diagnostic biomarker and therapeutic target in HCC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Deficiency of histone H3K36 methyltransferase SETD2 inhibits proliferation and migration of hepatocellular carcinoma through ERK pathway

Yang,

Zhang,

Munyurangabo

et al. 2023

Preprint

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“…biomarker, circular RNA, miRNA, non-coding RNA, prostate cancer various cancers such as liver, 7,8 lung, 9,10 stomach, 11,12 bladder, 13,14 and cervical cancers, 15,16 etc. Similarly, in PCa, an increasing number of circRNAs have been discovered.…”

Section: Introductionmentioning

confidence: 99%

“…Circular RNA (circRNA) is a special class of non‐coding RNA that is circular in shape and is formed by back splicing between the 5′ splice donor and the 3′ splice acceptor of the precursor messenger RNA. 6 Currently, many experiments have demonstrated that circRNAs play a crucial role in the development and progression of various cancers such as liver, 7 , 8 lung, 9 , 10 stomach, 11 , 12 bladder, 13 , 14 and cervical cancers, 15 , 16 etc. Similarly, in PCa, an increasing number of circRNAs have been discovered.…”

Section: Introductionmentioning

confidence: 99%

has_circ_0070512 promotes prostate cancer progression by regulating the miR‐338‐3p/hedgehog signaling pathway

et al. 2022

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Circular RNAs (circRNAs) are a type of non‐coding RNA that plays a vital role in biology. circRNAs appear to have a role in the development and progression of several malignancies, according to research. However, circRNAs that regulate prostate cancer (PCa) progression are still largely unknown and deserve further exploration. The aim of this study was to investigate the effect of hsa_circ_0070512 on the function and mechanism of PCa. hsa_circ_0070512 was increased in PCa tissues and cells and was mostly found in the cytoplasm of PCa cells. Overexpression of hsa_circ_0070512 considerably increased PCa cell proliferation and migration, whereas silencing of hsa_circ_0070512 greatly decreased PCa cell proliferation and migration. Mechanistically, we show that hsa_circ_0070512 acts as a “molecular sponge” for miR‐338‐3p and that the miR‐338‐3p mimics partially block the pro‐tumor effects of hsa_circ_0070512. RNA sequencing analysis of PC3 cells stably overexpressing hsa_circ_0070512 revealed that hedgehog was downstream of the signaling pathways of hsa_circ_0070512 and miR‐338‐3p. Our results implied that hsa_circ_0070512 regulated the hedgehog signaling pathways through miR‐338‐3p to enhance PCa growth and migration, providing a new diagnostic and therapeutic target for PCa.

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Recent progress in molecular mechanisms of postoperative recurrence and metastasis of hepatocellular carcinoma

Niu¹,

Wang²,

Niu³

2022

World J Gastroenterol

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Circular RNA circ SET domain containing 2 (circSETD2) inhibits hepatocellular carcinoma cell proliferation and invasion in vivo and in vitro

Cited by 3 publications

References 25 publications

Deficiency of histone H3K36 methyltransferase SETD2 inhibits proliferation and migration of hepatocellular carcinoma through ERK pathway

Deficiency of histone H3K36 methyltransferase SETD2 inhibits proliferation and migration of hepatocellular carcinoma through ERK pathway

has_circ_0070512 promotes prostate cancer progression by regulating the miR‐338‐3p/hedgehog signaling pathway

Recent progress in molecular mechanisms of postoperative recurrence and metastasis of hepatocellular carcinoma

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