RACO‐1 modulates Hippo signalling in oesophageal squamous cell carcinoma

Pang, Dan; Wang, Weilong; Zhou, Xiaofeng; Lu, Kui; Zhang, Jinghang; Chen, Zhiguo; Wang, Lingchao; Shen, Fangfang; Chen, Zhe; Wang, Sujie; Hou, Jinghan; Zhang, Aijia; Lv, Benjie; Gao, Can; Yan, Zhe; Hu, Yuhan; Chang, Tingmin; Wang, Lidong; Li, Xiumin

doi:10.1111/jcmm.15811

Cited by 8 publications

(7 citation statements)

References 26 publications

(65 reference statements)

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“…For example, PARK2 promoted YAP1 ubiquitination through proteasome-dependent degradation in esophageal squamous carcinoma [ 21 ]. RACO-1 promoted proteasome-dependent YAP1 degradation via inducing YAP1 K48-linked poly-ubiquitination and inhibiting YAP1 K63-linked poly-ubiquitination [ 22 ]. Additionally, HJURP can also regulate the ubiquitination of various proteins [ 8 , 23 ].…”

Section: Discussionmentioning

confidence: 99%

HJURP regulates cell proliferation and chemo-resistance via YAP1/NDRG1 transcriptional axis in triple-negative breast cancer

et al. 2022

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Triple-negative breast cancer is still a difficult point in clinical treatment at present, and a deep study of its pathogenesis has great clinical value. Therefore, our research mainly focuses on exploring the progression of triple-negative breast cancer and determines the important role of the HJURP/YAP1/NDRG1 transcriptional regulation axis in triple-negative breast cancer. We observed significantly increased HJURP expression levels in triple-negative breast cancer compared to other subtypes. HJURP could affect the level of ubiquitination modification of YAP1 protein and then regulate its downstream transcriptional activity. Mechanistically, we found that YAP1 positively regulates NDRG1 transcription by binding the promoter region of the NDRG1 gene. And HJURP/YAP1/NDRG1 axis could affect cell proliferation and chemotherapy sensitivity in triple-negative breast cancer. Taken together, these findings provide insights into the transcriptional regulation axis of HJURP/YAP1/NDRG1 in triple-negative breast cancer progression and therapeutic response.

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Section: Discussionmentioning

confidence: 99%

HJURP regulates cell proliferation and chemo-resistance via YAP1/NDRG1 transcriptional axis in triple-negative breast cancer

et al. 2022

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“…The role of RNF187 in different tumours remains controversial. While RNF187 exhibits tumour-suppressive activities in oesophageal squamous cell carcinoma [ 22 ] and triple-negative breast cancer, [ 19 ] ectopic RNF187 expression predicts a poor outcome and contributes to tumour progression in lung cancer, [ 16 ] hepatocellular carcinoma, [ 17 ] osteosarcoma [ 26 ] and ovarian carcinoma. [ 27 ] This discrepancy may be due to the differential substrates targeted by RNF187 in different cell types.…”

Section: Discussionmentioning

confidence: 99%

“…[ 20 , 21 , 28 ] However, two independent studies reported that RNF187 catalyses a K48 poly-ubiquitination in YAP for degradation, thus inhibiting the migration and invasion in oesophageal and breast cancer. [ 19 , 22 ] The role of RNF187 in progression of CRC is still unknown, despite transgenic overexpression of RACO‑1 coordinating K-Ras to cause hyperproliferation of colonic epithelium. [ 28 ] The present study revealed that the expression of RNF187 is significantly upregulated in CRC, which predicts a poor prognosis in CRC patients.…”

Section: Discussionmentioning

confidence: 99%

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Dysregulation of miR-144-5p/RNF187 axis contributes to the progression of colorectal cancer

Gao

Jiang

Hou

et al. 2022

Journal of Translational Internal Medicine

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Background and Objectives RING finger protein 187 (RNF187) belongs to RING domain-containing E3 ligases family, which was recently reported to be involved in oncogenesis and development of several cancers. This research aims to clarify the role of RNF187 in colorectal cancer (CRC) development. Methods The expression of RNF187 and miR-144-4p were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The levels of RNF187 protein were assessed by western blot analysis. Cell Counting Kit-8 (CCK8) assay, clonogenic assay, cell scratch test and transwell assay were used to determine the proliferation, migration and invasion of CRC cells in vitro. The binding of miR-144-5p and RNF197 mRNA was validated by luciferase reporter assays. Tumor-bearing nude mice were used to determine CRC cells growth in vivo. Results RNF187 expression significantly increased in CRC specimens and cell lines compared to normal colon tissues and normal colonic mucosa cell line, respectively. Upregulation of RNF187 expression was inversely correlated to poor prognosis in CRC patients. In addition, knockdown of RNF187 expression inhibited the proliferation, migration, and invasion but promoted the apoptosis of CRC lines Caco-2 and SW480 cells. Further studies validated that RNF187 was the direct target of miR-144-5p. The expression of miR-144-5p was downregulated in CRC tissues, which was negatively correlated to the expression of RNF187. Restoration of miR-144-5p significantly inhibited the progression of CRC cells and its anti-tumor effects could be abrogated by overexpression of RNF187. Conclusion Our findings demonstrate the deregulation of miR-144-5p/ RNF187 axis in CRC, as well as its role in regulation of the tumor progression, thus providing a novel therapeutic strategy for CRC treatment.

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“…On the other hand, YAP was regarded as a candidate oncogene in ESCC decades ago (20). Although many new regulators that play a part in modulating YAP activity have been identified in ESCC, such as RACO-1, PARK2, SHARPIN and SOX9 (39)(40)(41)(42). Whether C12orf59 alters YAP activity in ESCC remains unknown.…”

Section: Discussionmentioning

confidence: 99%

C12orf59 Promotes Esophageal Squamous Cell Carcinoma Progression via YAP-Mediated Epithelial-Mesenchymal Transition

Lin

et al. 2022

Front. Oncol.

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C12orf59 is a novel gene widely expressed in diverse normal human tissues. Aberrant expression of C12orf59, which is involved in tumor progression, has been reported in a few types of cancer. However, its expression and biological function in esophageal squamous cell carcinoma (ESCC) remain largely unclear. Here, we found that the mRNA and protein levels of C12orf59 were prominently higher in both tumor tissues and most ESCC cell lines. Functionally, C12orf59 overexpression promoted ESCC cell proliferation, migration and invasion, whereas C12orf59 depletion worked oppositely. Mechanistically, C12orf59 exerted its oncogenic function through the induction of epithelial-mesenchymal transition (EMT) of ESCC cells, which relied on Yes-associated protein (YAP) dephosphorylation and nuclear translocation. Constitutively active YAP further facilitated cell migration, invasion and EMT induced by enforced C12orf59 overexpression. On the contrary, increased cell motility and EMT caused by enforced C12orf59 overexpression were dramatically repressed upon YAP inactivation by verteporfin. Thus, we conclude that YAP activation driven by C12orf59 contributes to the malignancy of ESCC through EMT and that targeting drugs for C12orf59 combined with YAP inhibitor may be a potential therapeutic strategy for ESCC.

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RACO‐1 modulates Hippo signalling in oesophageal squamous cell carcinoma

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 8 publications

References 26 publications

HJURP regulates cell proliferation and chemo-resistance via YAP1/NDRG1 transcriptional axis in triple-negative breast cancer

HJURP regulates cell proliferation and chemo-resistance via YAP1/NDRG1 transcriptional axis in triple-negative breast cancer

Dysregulation of miR-144-5p/RNF187 axis contributes to the progression of colorectal cancer

C12orf59 Promotes Esophageal Squamous Cell Carcinoma Progression via YAP-Mediated Epithelial-Mesenchymal Transition

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