Cancer‐testis gene <scp><i>STK31</i></scp> is regulated by methylation and promotes the development of pancreatic cancer

Gao, Hao; Cai, Baobao; Lu, Zipeng; Wang, Guangfu; Gao, Yong; Miao, Yi; Jiang, Kuirong; Zhang, Kai

doi:10.1002/cam4.5472

Cited by 2 publications

(2 citation statements)

References 31 publications

(78 reference statements)

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“…STK31 has been implicated in promoting the progression of pancreatic cancer by enhancing cell proliferation, migration, and invasion. High expression of STK31 is associated with a poor prognosis in pancreatic cancer [44]. Previous studies have reported that PLA2G2F is a major secretory phospholipase A2 (sPLA2) expressed in the epidermis across different species, and its expression increases during epidermal hyperplasia.…”

Section: Rt-qpcr Validation For the Expression Of Pla2g2f Hhip Tnxb A...mentioning

confidence: 99%

Identification and Validation of a Prognostic Signature of m 5 C-Related Genes for Esophageal Cancer

Huang,

Wang,

Lin

et al. 2023

Preprint

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Background Esophageal cancer (ESCA) is a prevalent form of cancer with a grim prognosis. It has been reported that 5-methylcytosine (m5C) regulators are closely linked to carcinogenesis and distant metastasis. However, the role of m5C regulator in ESCA is still elusive. The aim of this study was to investigate the connections between m5C regulators and the initiation and progression of ESCA, with a particular focus on prognosis. Methods Gene expression profile data from TCGA database, including 11 normal and 142 tumor tissues, were obtained and divided into two ESCA subtypes according to the m5C regulators expression. Differentially expressed genes (DEGs) of two ESCA subtypes, normal and tumor tissues from TCGA, and normal and tumor tissues from validation datasets were analyzed. Inter-DEGs were filtered from the overlap of three sets of DEGs which named inter-DEGs. Functional analysis, immune infiltration analysis, drug sensitivity analysis, prognosis model was carried out to investigate the biological function and potential role of m5C regulators in ESCA. The expression of PLA2G2F, HHIP, TNXB, and STK31 in ESCA and adjacent esophageal tissues was detected by RT-qPCR. Results The expression of m5C regulators, namely TRDMT1, NSUN2, NSUN4, NSUN6, DNMT1, ALYREF, and YBX1, were upregulated in ESCA subtype 2 group. Correlation analysis demonstrated that m5C regulators positively correlated with E2F targets, G2M checkpoint, MYC targets V1, while negatively correlated with TNF-α signaling via NF-kB, and Notch signaling pathway. Additionally, the immune infiltration analysis indicated that m5C regulators was positively correlated with Macrophages M0, and negatively correlated with T cells CD8 infiltration. 4 independent prognostic genes, including PLA2G2F, HHIP, TNXB, and STK31, were selected to construct prognostic model and exhibited good function in predicting the prognosis of ESCA patients. RT-qPCR was used to validate the gene expression that the PLA2G2 had higher expression in ESCA tissues compared to adjacent tissues, while the expression of STK31, HHIP, and TNXB showed down regulation in ESCA tissues. Conclusions This study explored the comprehensive feature of 2 subtypes of m5C regulators in ESCA patients, which may improve understanding of m5C regulation in the tumor biology of ESCA.

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Section: Rt-qpcr Validation For the Expression Of Pla2g2f Hhip Tnxb A...mentioning

confidence: 99%

Identification and Validation of a Prognostic Signature of m 5 C-Related Genes for Esophageal Cancer

Huang,

Wang,

Lin

et al. 2023

Preprint

View full text Add to dashboard Cite

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“…STK31, also known as TDRD8, is a serine/threonine kinase that contains STK and Tudor domains. STK31 has been identified as a novel cancer testis antigen and has been shown to play an oncogenic role in various cancers, including colorectal, lung, pancreatic, and gastric (23)(24)(25). In lung cancer, STK31 was reported to induce lung cancer cell proliferation through the Wnt signaling pathway (26).…”

Section: Introductionmentioning

confidence: 99%

The molecular mechanism underlying KRAS regulation on STK31 expression in Pancreatic ductal adenocarcinoma

Chen,

Yuting,

Tang

et al. 2023

Preprint

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KRAS mutations are common in pancreatic ductal adenocarcinoma (PDAC) but targeting mutant KRAS is still challenging. Kinase inhibitors are ideal targeted therapeutics for mutant KRAS-driven cancer. In our study, an esiRNA screening was performed to identify kinases that play a critical role in KRAS mutant driven PDAC. STK31 was identified as a potential therapeutic target for KRAS mutant PDAC. In this study, we aimed to investigate the underlying mechanism of STK31 in KRAS mutant PDAC and its therapeutic potential. Our results showed that STK31 was upregulated in KRAS mutant PDAC patients with poor survival and highly expressed in PDAC cell lines with KRAS G12D mutant background. Inhibition of STK31 in KRAS mutant cell lines significantly reduced PDAC cell growth and hindered in vivo tumor growth. Gain and loss of function experiments revealed that STK31 is a downstream target of KRAS in PDAC. Pharmacological inhibition assay showed MAPK/ERK signaling involved in STK31 regulation. The further mechanistic study validated that c-Jun, regulated by KRAS/MAPK signaling, directly modulates the transcription level of STK31 by binding to its promoter region. By analyzing RNA sequencing data, we found cell cycle regulators CCNB1 and CDC25C are downstream targets of STK31. Our results indicate that STK31 promotes PDAC cell growth by regulating the KRAS/MAPK/ERK/c-Jun signaling pathway and its impact on cell cycle regulator CCNB1.

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Cancer‐testis gene STK31 is regulated by methylation and promotes the development of pancreatic cancer

Cited by 2 publications

References 31 publications

Identification and Validation of a Prognostic Signature of m 5 C-Related Genes for Esophageal Cancer

Identification and Validation of a Prognostic Signature of m 5 C-Related Genes for Esophageal Cancer

The molecular mechanism underlying KRAS regulation on STK31 expression in Pancreatic ductal adenocarcinoma

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