Evidence map›Paper›PMID 39347031›Full record

ArticleJournal of dental sciences2024

Protein inhibitor of activated signal transducer and activator of transcription 2 is an oncoprotein in oral squamous cell carcinoma and related to cigarette smoking - An in vitro study.

Szu-Yu Chen, Chi-Fu Chiang, Yu-Fu Su, Che-Yi Lin, Yi-Jen Hung, Tsai-Wang Huang, Yi-Shing Shieh

Abstract read
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Article in Journal of dental sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Szu-Yu ChenGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Chi-Fu ChiangGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Yu-Fu SuDepartment of Radiation Oncology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Che-Yi LinDepartment of Oral and Maxillofacial Surgery, Chi Mei Medical Center, Tainan, Taiwan.
Yi-Jen HungDivision of Endocrinology and Metabolism, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Tsai-Wang HuangDivision of Thoracic Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Yi-Shing ShiehDepartment and Graduate Institute of Biochemistry, National Defense Medical Center, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/purpose: Oral cancer is one of the most prevalent malignant tumors in Taiwan. Due to the heterogeneity of oral cancer cells, the five-year survival rate of patients is only 50%. Post-translational modifications contribute to protein diversity and directly influence cell functions. The protein inhibitor of activated signal transducer and activator of transcription 2 (PIAS2) is known to undergo post-translational modifications, yet its impact on oral cancer remains unclear. Materials and methods: PIAS2 expression was modulated by transfecting cells with a PIAS2 expression vector or by knocking down PIAS2 using siRNA with low and high PIAS2 expression, respectively. These cells were subjected to invasion, migration, and proliferation assays to evaluate the effects of PIAS2. Changes in genotype, such as epithelial-mesenchymal transition (EMT) markers, were also examined. Additionally, the effect of cigarette smoke condensate (CSC) on PIAS2 expression in oral squamous cell carcinoma (OSCC) cells was investigated. Results: Overexpression of PIAS2 significantly increased the malignant behaviors of oral cancer cells. In YD38 and SAS cells with low PIAS2 expression, overexpression of PIAS2 enhanced proliferation, invasion, and migration. PIAS2 overexpression also affected EMT gene expression, suppressing E-cadherin and increasing fibronectin expression. Conversely, PIAS2 knockdown in OECM1 and SCC25 cells suppressed malignant behaviors and reversed EMT markers, increasing E-cadherin and decreasing fibronectin expression. Furthermore, a dose-dependent increase in PIAS2 expression was observed when OSCC cells were treated with CSC. Conclusion: PIAS2 functions as an oncogene in oral cancer, and cigarette smoking induces PIAS2 expression. Increased PIAS2 levels lead to enhanced malignancy in oral cancer.

Indexed as

Cigarette smoke condensateEpithelial-mesenchymal transitionOncoproteinOral squamous cell carcinomaProtein inhibitor of activated STAT 2

Identifiers

PMID39347031
PMCPMC11437306

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.