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Background <p>Cancer remains a leading cause of mortality worldwide, characterized by complex genetic and molecular alterations. The Protein Tyrosine Phosphatase Non-Receptor Type 6 (PTPN6), also known as SHP-1, plays a critical role in regulating immune responses and cellular signaling pathways, with emerging evidence suggesting its involvement in cancer progression. Previous studies have linked aberrant PTPN6 expression to tumorigenesis in specific cancers, such as lymphoma and leukemia, where it acts as a tumor suppressor. However, the comprehensive role of PTPN6 across pan-cancer, particularly its prognostic significance and molecular functions, has not been fully elucidated.</p> Methodology <p>This study aimed to provide a pan-cancer analysis of PTPN6, utilizing data from multiple public databases with molecular in vitro experiments.</p> Results <p>Our findings showed notable differences in PTPN6 expression among different cancer types. Prognostic analyses indicated that higher PTPN6 expression is associated with poorer overall survival in with notable upregulation in kidney renal clear cell carcinoma (KIRC), liver hepatocellular carcinoma (LIHC), and rectum adenocarcinoma (READ). Further, promoter methylation and mutation analyses highlighted alterations in PTPN6 expression across different cancer stages, with a particular reduction in methylation observed in tumor tissues. Functional assays in cell lines demonstrated that PTPN6 promotes cell proliferation, migration, and colony formation, supporting its role in cancer progression.</p> Conclusion <p>This comprehensive analysis emphasizes the potential of PTPN6 as both a prognostic biomarker and a therapeutic target in cancer. However, further research is required to fully elucidate its role in cancer progression and to assess its clinical applicability.</p>

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Pan-cancer analysis of PTPN6: prognostic significance and functional implications in tumor progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月25日

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  • Xiaohui Wang,
  • Mumtaz Hussain,
  • Qurat ul Ain,
  • Madiha Zaynab,
  • Mostafa A. Abdel-Maksoud,
  • Taghreed N. Almana,
  • Saeedah Almutair,
  • Abdulaziz Alamri,
  • Ibrahim A. Saleh,
  • Naser Zomot,
  • Wahidah H. Al-Qahtani,
  • Faisal Siddique,
  • Yasir Hameed

摘要

Background

Cancer remains a leading cause of mortality worldwide, characterized by complex genetic and molecular alterations. The Protein Tyrosine Phosphatase Non-Receptor Type 6 (PTPN6), also known as SHP-1, plays a critical role in regulating immune responses and cellular signaling pathways, with emerging evidence suggesting its involvement in cancer progression. Previous studies have linked aberrant PTPN6 expression to tumorigenesis in specific cancers, such as lymphoma and leukemia, where it acts as a tumor suppressor. However, the comprehensive role of PTPN6 across pan-cancer, particularly its prognostic significance and molecular functions, has not been fully elucidated.

Methodology

This study aimed to provide a pan-cancer analysis of PTPN6, utilizing data from multiple public databases with molecular in vitro experiments.

Results

Our findings showed notable differences in PTPN6 expression among different cancer types. Prognostic analyses indicated that higher PTPN6 expression is associated with poorer overall survival in with notable upregulation in kidney renal clear cell carcinoma (KIRC), liver hepatocellular carcinoma (LIHC), and rectum adenocarcinoma (READ). Further, promoter methylation and mutation analyses highlighted alterations in PTPN6 expression across different cancer stages, with a particular reduction in methylation observed in tumor tissues. Functional assays in cell lines demonstrated that PTPN6 promotes cell proliferation, migration, and colony formation, supporting its role in cancer progression.

Conclusion

This comprehensive analysis emphasizes the potential of PTPN6 as both a prognostic biomarker and a therapeutic target in cancer. However, further research is required to fully elucidate its role in cancer progression and to assess its clinical applicability.