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Cell Transformation by PTP1B Truncated Mutants Found in Human Colon and Thyroid Tumors

Wenhan Mei1, Kemin Wang1, Jian Huang1

  • 1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory of Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, 200025, China.

Plos One
|November 18, 2016
PubMed

Insights

Mutated protein tyrosine phosphatase 1B (PTP1B) splice mutations were found in ~20% of colon and thyroid tumors. A PTP1B mutant induced oncogenic transformation independently of Src, suggesting a novel therapeutic target for these cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Wild-type protein tyrosine phosphatase 1B (PTP1B) has a dual role in cancer, acting as either a tumor suppressor or promoter.
  • The role of mutated PTP1B in human carcinogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate the involvement of mutated PTP1B in human carcinogenesis.
  • To characterize the oncogenic potential of specific PTP1B splice mutants.

Main Methods:

  • Sequencing of PTP1B cDNAs from human tumors.
  • Expression and functional analysis of PTP1B splice mutants (PTP1BΔE6 and PTP1BΔE5) in rat fibroblasts.
  • Assessment of tumor formation in nude mice.

Main Results:

  • Splice mutations in PTP1B were identified in approximately 20% of colon and thyroid tumors.
  • The PTP1BΔE6 mutant, lacking phosphatase activity, induced oncogenic transformation of fibroblasts independently of Src signaling.
  • Transformed cells exhibited tumorigenicity in vivo, suggesting PTP1B mutations impact other cancer-related molecules.

Conclusions:

  • Mutated PTP1B plays a role in human carcinogenesis, particularly in colon and thyroid cancers.
  • The PTP1BΔE6 mutant possesses oncogenic properties through Src-independent pathways.
  • These findings highlight mutated PTP1B as a potential therapeutic target for specific cancers.

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