PTK7

Overview

PTK7 is a highly conserved but catalytically inactive receptor tyrosine kinase in the Wnt signaling pathway, which has been shown preclinically to be enriched on tumor initiating cells (TICs) in several tumor types.1


  • Protein tyrosine kinase 7 (PTK7) belongs to the receptor tyrosine kinase family with an inactive kinase domain2
  • PTK7, also known as colon carcinoma kinase 4 (CCK-4), is upregulated in various cancers, where it is known to act as either an oncoprotein or a tumor suppressor3

IMPLICATIONS IN CANCER

  • An unbiased analysis of isolated TIC populations provided the first indication that PTK7 is enriched on TICs.1
  • Next-generation whole transcriptome sequencing of functionally tumorigenic cell subpopulations showed higher PTK7 expression on TICs from triple negative breast cancer (TNBC) and ovarian cancer patient-derived xenografts compared to normal tissues.1
  • PTK7 is also highly overexpressed in a variety of tumors, such as colon cancer, lung adenocarcinoma, acute myelogenous leukemia, and gastric cancer.2

Oncogenic Expression1

An analysis to quantify the PTK7 protein in a panel of protein lysates from TNBC, ovarian, and NSCLC patient derived xenografts and a panel of normal tissues found:

TNBC

  • PTK7 expression was observed in 12 of 12 (100%) patient-derived xenografts.

NSCLC

  • Higher PTK7 expression in NSCLC is associated with significantly shorter survival and it was observed that PTK7 enriches for TICs in NSCLC.

Ovarian

  • PTK7 expression was observed in 43 of 47 (91%) patient-derived xenografts.
  1. Damelin M, et al. A PTK7-targeted antibody-drug conjugate reduces tumor-initiating cells and induces sustained tumor regressions. Sci Transl Med. 2017;9(372). pii: eaag2611.
  2. Sun J-J, et al. The increased PTK7 expression is a malignant factor in cervical cancer. Hindawi Disease Markers. Volume 2019. Article ID 5380197. 10 pages.
  3. Shin W-S, et al. Biphasic regulation of tumorigenesis by PTK7 expression level in esophageal squamous cell carcinoma. Scientific Reports. Volume 8. Article number: 8519 (2018).

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