The Role of CT10 Regulation of Kinase-Like in Cancer

Abstract

V-crk avian sarcoma virus CT10 oncogene homolog-like (CRKL) is a member of CRK family. It acts as an adaptor protein in intracellular signal transduction. CRKL has been reported overexpressed in a variety of cancers affecting the aggressive and malignant behaviors of cancer cells. CRKL seems to show a tumor-promotion role in gastric cancer, glioblastoma multiforme, hepatocellular carcinoma, bladder cancer, lung cancer, colon cancer, ovarian cancer, leukemia, breast cancer, head and neck cancer, rhabdomyosarcoma and neuroblastoma. The association of CRKL with malignant tumors and its potential action mechanisms were summarized. CRKL has the potential to be used as a biomarker for the diagnosis, treatment and prognosis of certain tumors.

CrkL meditates CCL20/CCR6-induced EMT in gastric cancer

“…In addition, CrkL acts as an adaptor protein to induce the intracellular signal transduction [8,9]. As reported, CrkL is also highly expressed in different cancer cells, such as gastric cancer, glioblastoma, hepatocellular carcinoma, and implicated in the aggressiveness and transformation of malignance [10,11].…”

Crk-like adapter protein regulates CCL19/CCR7-mediated epithelial-to-mesenchymal transition via ERK signaling pathway in epithelial ovarian carcinomas

“…CrkL is a member of the human Crk adapter protein family, which is comprised of two alternatively spliced isoforms of CRK, the human homologue of the avian sarcoma retroviral v-crk oncogene [5,6]. CrkL is best known as a key substrate and effective downstream molecule of the BCR-ABL1 oncogenic tyrosine kinase in breast cancer [7] and bladder cancer [8].…”

CRKL knockdown promotes in vitro proliferation, migration and invasion, in vivo tumor malignancy and lymph node metastasis of murine hepatocarcinoma Hca-P cells

“…CRKL deregulation is linked to the development and progression of a variety of cancers [21][22][23]. As we summarized in our review [22], CRKL abnormal expression is associated with gastric cancer (GC), glioblastoma multiforme (GBM), hepatocellular carcinoma (HCC), bladder cancer, lung cancer, colon cancer, ovarian cancer, leukemia, breast cancer, head and neck cancer, rhabdomyosarcoma and neuroblastoma.…”

“…As we summarized in our review [22], CRKL abnormal expression is associated with gastric cancer (GC), glioblastoma multiforme (GBM), hepatocellular carcinoma (HCC), bladder cancer, lung cancer, colon cancer, ovarian cancer, leukemia, breast cancer, head and neck cancer, rhabdomyosarcoma and neuroblastoma. It is of promise as an indicator for cancer development, invasion and metastasis as well as an attractive target for the diagnostics and prognosis of cancer [22,23]. Recently, we found CRKL was linked to the lymphatic metastasis of hepatocarcinoma [23].…”

“…CRKL commonly localizes in multiple intracellular compartments mapped at 22q11.21 encoding a protein of 36 kDa [14]. CRKL deregulation is involved in the development and progression of a variety of cancers including gastric cancer (GC), glioblastoma multiforme (GBM), hepatocellular carcinoma (HCC), bladder cancer, lung cancer, colon cancer, ovarian cancer, leukemia, breast cancer, head and neck cancer, rhabdomyosarcoma and neuroblastoma [15][16][17][18][19][20][21][22]. Nevertheless, the role and action mechanism of CRKL in tumor progression are still unclear.…”