1. Academic Validation
  2. PTP1B promotes the malignancy of ovarian cancer cells in a JNK-dependent mechanism

PTP1B promotes the malignancy of ovarian cancer cells in a JNK-dependent mechanism

  • Biochem Biophys Res Commun. 2018 Sep 5;503(2):903-909. doi: 10.1016/j.bbrc.2018.06.094.
Wenyan Wang 1 Yunxia Cao 2 Xiao Zhou 3 Bing Wei 4 Yu Zhang 4 Xiaochun Liu 5
Affiliations

Affiliations

  • 1 Department of Obstetrics &Gynecology, The Second Hospital of Anhui Medical University, Hefei City, Anhui Province, 230601, PR China; Teaching and Research Group of Obstetrics & Gynecology, Anhui Medical University, Hefei City, Anhui Province, 230032, PR China.
  • 2 Teaching and Research Group of Obstetrics & Gynecology, Anhui Medical University, Hefei City, Anhui Province, 230032, PR China. Electronic address: nlrlnv1@163.com.
  • 3 Department of Cardiothoracic Surgery, The Second Hospital of Anhui Medical University, Hefei City, Anhui Province, 230601, PR China.
  • 4 Department of Obstetrics &Gynecology, The Second Hospital of Anhui Medical University, Hefei City, Anhui Province, 230601, PR China.
  • 5 Department of Obstetrics & Gynecology, Shanxi Academy of Medical Sciences & Shanxi Da Yi Hospital, Taiyuan, Shanxi, 030032, PR China.
Abstract

Ovarian Cancer is the leading cause of death from gynecological malignancies in women. Diagnosis at the early stage remains challenging and efficient treatment is still highly needed. The development and progression of this Cancer is associated with many genetic and epigenetic changes, representing the dysregulation of a highly complex signaling network. Previous studies found that protein-tyrosine Phosphatase 1 B (PTP1B) was aberrantly expressed in many types of ovarian Cancer cells. The exact role of this protein, however, remains controversial. We found that PTP1B was highly expressed in several ovarian carcinoma cell lines. Changing its expression level strongly affected the malignancy phenotypes of the cultured Cancer cells and growth of tumors in nude mice. Further analysis at the molecular level found that overexpression of PTP1B activated the JNK (c-Jun N-terminal kinase) signaling pathway and impacted a set of factors involved in Cancer metastasis. Overall, our study suggested that overexpression of PTP1B could be a driving factor in the tumorigenesis and progression of ovarian Cancer and restoring the normal expression level of this signaling molecule may represent a promising strategy in treating this disease.

Keywords

Invasion; JNK; Migration; Ovarian cancer; PTP1B.

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