circHIPK3 promotes oxaliplatin-resistance in colorectal cancer through autophagy by sponging miR-637

Zhang, Yanli; Li, Chen; Liu, Xinfeng; Wang, Yanlei; Zhao, Rui; Yang, Yongmei; Zheng, Xin; Zhang, Yi; Zhang, Xin

doi:10.1016/j.ebiom.2019.09.051

Cited by 102 publications

(74 citation statements)

References 59 publications

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“…Our research showed that circHIPK3, which mainly existed in the cytoplasm, was high-expressed in RC tissues and cells, and that knocking down circHIPK3 could inhibit the proliferation, migration and invasion of RC cells. Previous reports revealed that circHIPK3 is highexpressed in the tissues and cells of colon carcinoma, non-small cell lung carcinoma, and nasopharyngeal carcinoma [25][26][27]. However, Li et al [28] found that circHIPK3 is significantly down-regulated in bladder carcinoma cells and is negatively related to the classification, invasion of bladder carcinoma and lymph node metastasis.…”

Section: Discussionmentioning

confidence: 96%

CircHIPK3 promotes proliferation and metastasis and inhibits apoptosis of renal cancer cells by inhibiting MiR-485-3p

Lai

Xin

et al. 2020

Cancer Cell Int

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Background: The intervention of circHIPK3 in renal carcinoma (RC) has not been reported, and thus, the current study investigated the intervention and mechanism of circHIPK3 in RC. Methods: The expression of circHIPK3 in RC tissues and cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Ribonuclease R (RNase R) resistance and distribution of circHIPK3 and HIPK3 were analyzed by RNase R digestion experiments and cytoplasm/nucleus separation experiments. CircHIPK3 was knocked down in ACHN and 769-P cells. Cell counting kit-8 (CCK-8), colony formation assay, scratch assay, and Transwell assay were performed to detect cell proliferation and metastasis. CircInteractome, qRT-PCR and dual-luciferase reporter assay were used to predict the target miRNAs of circHIPK3. Furthermore, a series of rescue experiments were performed to analyze the regulatory relationship between circHIPK3 and miR-485-3p. Epithelial-mesenchymal transition (EMT) and the expressions of apoptosis-associated markers were detected by Western blot and qRT-PCR. The regulatory relationship between circHIPK3 and miR-485-3p in vivo was explored by xenograft experiments, Western blot, qRT-PCR and immunohistochemistry (Ki-67). Results: CircHIPK3 was mainly overexpressed in the cytoplasm of RC tissues and cells. Knocking down circHIPK3 inhibited the proliferation, migration, and invasion of RC cells. The expression of circHIPK3 was negatively related to that of its target gene miR-485-3p. Results of the rescue experiments showed that circHIPK3 overexpression could partially reverse the anti-carcinoma effect of miR-485-3p mimic. The specific mechanism of circHIPK3 was related to the effect of miR-485-3p on partially reversing the up-regulated expressions of Clever caspase-3, Bax, E-Cadherin and down-regulated expressions of Bcl-2, N-Cadherin and Vimentin. The results of in vivo experiments demonstrated that circHIPK3 promoted tumor growth and the expression of Ki-67 by down-regulating miR-485-3p. Conclusion: CircHIPK3 promotes the proliferation and metastasis and inhibits the apoptosis of RC cells through competitively binding to miR-485-3p.

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Section: Discussionmentioning

confidence: 96%

CircHIPK3 promotes proliferation and metastasis and inhibits apoptosis of renal cancer cells by inhibiting MiR-485-3p

Lai

Xin

et al. 2020

Cancer Cell Int

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“…CDK6, STAT3, AKT1) ( Table 2). In addition, miR-637 could be itself regulated by non-coding endogenous competitors other than solely circHIPK3, as described in other diseases (26)(27)(28)(29)(30)(31)(32)(33)(34) (Table 2).…”

Section: A Comprehensive Analysis Of Circ-0000284 (Circhipk3) In Ccamentioning

confidence: 93%

Exosomal circRNAs: new players in the field of cholangiocarcinoma

2019

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Cholangiocarcinoma (CCA) is a deadly cancer worldwide associated with limited therapeutic options. A recent study published in Clinical Science by Wang and colleagues [Clin. Sci. (2019) 133(18), 1935–1953] brought new perspectives to CCA management and therapy by focusing on circular RNAs (circRNAs). CircRNAs belong to an emerging class of functional non-coding RNAs (ncRNAs) regulating numerous biological processes. Notably, circRNAs have been associated with cancer onset and progression, although reports in CCA are very limited so far. In this work, the expression of circular RNA circ-0000284 (aka circHIPK3) was specifically elevated in CCA cell lines, human tumor tissues and plasma exosomes. Gain and loss of function approaches were performed to better understand the molecular mechanisms regulated by circ-0000284. Notably, the authors evaluated the role of circ-0000284 as a microRNA (miRNA) sponge. By prediction analysis and functional tests, a direct interaction was demonstrated with miR-637 that targets lymphocyte antigen-6 E (LY6E). Increased expression of circ-0000284 was associated with enhanced migration, invasion and proliferation of CCA cell lines. Interestingly, exosomal-mediated circ-0000284 was reported to exhibit pro-oncogenic effects on surrounding normal cells. Altogether, these data highlight circRNAs not only as new players in CCA pathogenesis but also as promising molecules for innovative non-invasive biomarkers, as circRNAs are enriched and stable in exosomes. Further investigations on extracellular vesicles should provide the necessary tools to improve CCA diagnosis, and move toward targeted-therapies.

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“…We previously confirmed that microRNA-637 (miR-637) is a favorable prognosis marker in glioma that targets the 3ʹ-untranslated region (UTR) of Akt1 (13). Further targets of miR-637, such as signal transducer and activator of transcription 3 (STAT3) and nuclear protein 1 (NUPR1) (14,15), have been validated so far, but there remains a lack of knowledge regarding upstream regulation.…”

Section: Introductionmentioning

confidence: 94%

Oncogenic ZEB2/miR-637/HMGA1 signaling axis targeting vimentin promotes the malignant phenotype of glioma

Zeng

Que

Lin

et al. 2020

Preprint

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Background Glioma is the most common primary tumor of the central nervous system. We previously confirmed that zinc finger E-box binding homeobox (ZEB) 2 promotes the malignant progression of glioma, while microRNA-637 (miR-637) is associated with favorable prognosis in glioma. This study investigated the potential interaction between ZEB2 and miR-637 and its downstream signaling pathway in glioma. Methods Chromatin immunoprecipitation, luciferase reporter, and electrophoretic mobility shift assays were used to confirm ZEB2 binding to miR-637. Microarray and bioinformatic analyses were used to investigate targets of miR-637. MTT and EdU assays, transwell assays, and Boyden assays were utilized to assess cell viability, migration, and invasion, respectively. A subcutaneous xenograft model was utilized for analyzing the role of miR-637/high mobility group A1 (HMGA1) interaction in vivo. Immunohistochemistry staining of clinical samples and bioinformatic analysis of the Chinese Glioma Genome Atlas and The Cancer Genome Atlas databases were performed to further confirm the ZEB2/miR-637/HMGA1/vimentin axis. Results ZEB2 was bound directly bind to the E-box elements in the miR-637 promoter and promoted cell proliferation, migration, and invasion via miR-637 downregulation. Subsequent screening confirmed that HMGA1 was a direct target of miR-637, while miR-637 could propagate the malignant phenotype of glioma by suppressing HMGA1 both in vitro and in vivo. Furthermore, the interaction between cytoplasmic HMGA1 and vimentin was observed, and vimentin inhibition could abolish increased migration and invasion induced by HMGA1 overexpression. Notably, the ZEB2/miR-637/HMGA1/vimentin axis was also evident in glioma tissue samples and public glioma datasets, while both HMGA1 and vimentin were associated with an unfavorable prognosis in glioma. Additionally, upregulated HMGA1 and vimentin were found in isocitrate dehydrogenase (IDH) wild-type and 1p/19q non-codeletion diffusely infiltrating glioma. Conclusions We identified an oncogenic ZEB2/miR-637/HMGA1 signaling axis targeting vimentin that promotes both migration and invasion in glioma. This not only extends the current understanding of miR-637 regulation in glioma, but also unravels a novel signaling pathway that integrates a transcriptional factor, microRNA, and a chromatin remodeling factor to modulate the malignant phenotype of glioma.

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circHIPK3 promotes oxaliplatin-resistance in colorectal cancer through autophagy by sponging miR-637

Cited by 102 publications

References 59 publications

CircHIPK3 promotes proliferation and metastasis and inhibits apoptosis of renal cancer cells by inhibiting MiR-485-3p

CircHIPK3 promotes proliferation and metastasis and inhibits apoptosis of renal cancer cells by inhibiting MiR-485-3p

Exosomal circRNAs: new players in the field of cholangiocarcinoma

Oncogenic ZEB2/miR-637/HMGA1 signaling axis targeting vimentin promotes the malignant phenotype of glioma

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