<i>RETRACTED:</i> YY1 suppresses proliferation and migration of pancreatic ductal adenocarcinoma by regulating the CDKN3/MdM2/P53/P21 signaling pathway

Liu, Dongfang; Zhang, Jingjing; Wu, Yang; Shi, Guodong; Hao, Yuan; Lu, Zipeng; Zhu, Qing; Wu, Pengfei; Lü, Cheng; Guo, Feng; Chen, Jianmin; Jiang, Kuirong; Miao, Yi

doi:10.1002/ijc.31173

Cited by 64 publications

(49 citation statements)

References 43 publications

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“…However, previous studies have reported contradictory effects of CDKN3 on the cell cycle. Some studies have shown that CDKN3 acts as a cancer-promoting gene in a variety of ways to regulate the G1/S phase transition [40,41], while others have reported that CDKN3 plays an anti-tumour role via dephosphorylation of CDK2, thereby inhibiting the G1/S phase transition [31]. Therefore, the specific regulatory mechanism by which CDKN3 influences the cell cycle remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics-based screening of key genes for transformation of liver cirrhosis to hepatocellular carcinoma

Chen

Yuan

et al. 2020

J Transl Med

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Background: Hepatocellular carcinoma (HCC) is the most common type of liver tumour, and is closely related to liver cirrhosis. Previous studies have focussed on the pathogenesis of liver cirrhosis developing into HCC, but the molecular mechanism remains unclear. The aims of the present study were to identify key genes related to the transformation of cirrhosis into HCC, and explore the associated molecular mechanisms.Methods: GSE89377, GSE17548, GSE63898 and GSE54236 mRNA microarray datasets from Gene Expression Omnibus (GEO) were analysed to obtain differentially expressed genes (DEGs) between HCC and liver cirrhosis tissues, and network analysis of protein-protein interactions (PPIs) was carried out. String and Cytoscape were used to analyse modules and identify hub genes, Kaplan-Meier Plotter and Oncomine databases were used to explore relationships between hub genes and disease occurrence, development and prognosis of HCC, and the molecular mechanism of the main hub gene was probed using Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway analysis. Results:In total, 58 DEGs were obtained, of which 12 and 46 were up-and down-regulated, respectively. Three hub genes (CDKN3, CYP2C9 and LCAT) were identified and associated prognostic information was obtained. CDKN3 may be correlated with the occurrence, invasion, and recurrence of HCC. Genes closely related to changes in the CDKN3 hub gene were screened, and Kyoto Encyclopedia of Genes and Genomes (KEGGs) pathway analysis identified numerous cell cycle-related genes.Conclusion: CDKN3 may affect the transformation of liver cirrhosis into HCC, and represents a new candidate molecular marker of the occurrence and progression of HCC.

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Section: Discussionmentioning

confidence: 99%

Bioinformatics-based screening of key genes for transformation of liver cirrhosis to hepatocellular carcinoma

Chen

Yuan

et al. 2020

J Transl Med

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“…It has been reported that YY1 is overexpressed and serves as oncogene in numerous tumor types, including breast, ovary, colon, prostate, gastric and laryngeal cancer (17)(18)(19)(20)(21). However, YY1 may serve an inhibitory role in pancreatic cancer (22). A recent study demonstrated that the expression of YY1 was significantly upregulated in differentiated thyroid and anaplastic cancer (23).…”

Section: Discussionmentioning

confidence: 99%

miR‑544 inhibits the migration and invasion of anaplastic thyroid cancer by targeting Yin Yang‑1

Wang

Sun

2019

Oncol Lett

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Anaplastic thyroid cancer (ATC), with a mean survival time of 6 months, was reported in 2012 to account for 1-2% of all thyroid tumor cases in the US. Understanding the molecular mechanisms underlying carcinogenesis and progression in ATC would contribute to determining novel therapeutic targets. The aberrant expression of microRNA-544 (miR-544) has been demonstrated in various cancer types. However, its expression and biological function in human ATC remain largely unknown. Therefore, the present study investigated the expression, function and molecular mechanism of miR-544 in ATC. Results of reverse transcription-quantitative polymerase chain reaction demonstrated that the expression levels of miR-544 in 40 pairs of surgical specimens and human ATC cell lines were significantly decreased, compared with the normal thyroid tissues and cell line. Functional assays indicated that ectopic expression of miR-544 significantly decreased the viability, proliferation and metastasis of SW1736 cells, whereas miR-544 inhibitor significantly enhanced the viability, proliferation and metastasis of 8305C cells. Furthermore, the present study confirmed that the oncogene Yin Yang-1 (YY1) was a direct target of miR-544. It was further demonstrated that YY1 overexpression rescued the inhibitory effect of progression induced by miR-544 in ATC cells. Finally, in vivo study indicated that miR-544 suppressed the tumorigenicity of ATC cells. In conclusion, the present study demonstrated that miR-544 may function as a tumor suppressor in ATC and serve as a future therapeutic target for patients with ATC.

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“…Altogether, Numb or p53 knockdown reversed the upregulation of wtp53 induced by silencing SRPK2 in response to oxaliplatin. p53 knockdown reversed the decrease in cell migration and invasion induced by SRPK2 silencing after treatment with oxaliplatin It is well known that p53 acts as a critical regulator in the malignant biology of various cancers [25,26]. Thus, we investigated whether SRPK2 promoted cell migration and invasion in a p53-dependent manner in PC cells.…”

Section: Srpk2 Regulated Cell Migration Invasion and Chemosensitivitmentioning

confidence: 96%

Serine/arginine protein‐specific kinase 2 promotes the development and progression of pancreatic cancer by downregulating Numb and p53

et al. 2019

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Serine/arginine protein‐specific kinase 2 (SRPK2) plays a vital role in the progression of a range of different malignancies, including pancreatic cancer. However, the mechanisms are poorly understood. Previous studies have shown that in hepatocellular carcinoma, SRPK2 knockdown leads to the upregulation of the cell fate determining protein Numb, and in pancreatic cancer cells, Numb knockdown prevents ubiquitin‐mediated degradation of p53. In this study, we investigated the relationship between SRPK2, Numb and p53 in the development of pancreatic cancer with or without chemical agent treatment in vitro. SRPK2 expression was upregulated in pancreatic cancer tissues and associated with decreased overall survival in pancreatic cancer patients, indicating that expression of this protein can be used as a marker of unfavourable prognosis. Expression of SRPK2 was positively associated with tumour T stage and Union for International Cancer Control (UICC) stage, and negatively associated with Numb expression in serial tissue sections. In pancreatic cancer cells, SRPK2 downregulation or overexpression led to modulation of Numb and wild‐type p53 protein expression in response to oxaliplatin treatment. Furthermore, these three endogenous proteins could be coimmunoprecipitated as a triple complex. Numb or p53 knockdown reversed the upregulation of p53 that was induced by silencing SRPK2. SRPK2 overexpression promoted cell invasion and migration, and decreased chemosensitivity of cancer cells to gemcitabine or oxaliplatin treatment. Conversely, SRPK2 silencing decreased cell invasion and migration and increased chemosensitivity; these effects were reversed by silencing p53 in oxaliplatin‐treated pancreatic cancer cells. Our data suggest that SRPK2 negatively regulates p53 by downregulating Numb under chemical agent treatment. Thus, SRPK2 promotes the development and progression of pancreatic cancer in a p53‐dependent manner.

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RETRACTED: YY1 suppresses proliferation and migration of pancreatic ductal adenocarcinoma by regulating the CDKN3/MdM2/P53/P21 signaling pathway

Cited by 64 publications

References 43 publications

Bioinformatics-based screening of key genes for transformation of liver cirrhosis to hepatocellular carcinoma

Bioinformatics-based screening of key genes for transformation of liver cirrhosis to hepatocellular carcinoma

miR‑544 inhibits the migration and invasion of anaplastic thyroid cancer by targeting Yin Yang‑1

Serine/arginine protein‐specific kinase 2 promotes the development and progression of pancreatic cancer by downregulating Numb and p53

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