IMR Press / FBL / Volume 19 / Issue 3 / DOI: 10.2741/4223

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Downregulation of CRKL expression can inhibit tumorigenesis in colon cancer
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1 Department of gastroenterology, the First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou 350005, Fujian Province, China
2 Department of Neurology, the Affiliated Union Hospital, Fujian Medical University, 29 Xinquan Rd, Fuzhou 350001, Fujian Province, China
3 Laboratory of Genetic Medicine and Immunology, Weill Cornell Medical College in Qatar – Qatar Foundation, Education City, P.O.Box 24144, Doha, Qatar
4 Department of Thoracic Surgery, Shanghai Pulmonary Hospital of Tongji University,507 Zhengmin Rd., Shanghai 200433, PR China
Front. Biosci. (Landmark Ed) 2014, 19(3), 528–534;
Published: 1 January 2014

CRKL, as a "switch" factor on several oncogenic pathways, plays vital roles in multiple cancers. However, little is known about CRKL in gastrointestinal cancers. Here, we showed that CRKL is involved in colon cancer, which is the most common form of cancer of the digestive system. Immunohistochemistry analysis showed that CRKL expression in colon tumor tissue is significantly higher than normal tissue and CRKL level is associated with tumor differentiation. Suppression of CRKL in colon cancer cells inhibited cell proliferation, migration and invasion, while induced apoptosis. Colon cancer cells xenografts in nude mice showed that CRKL promoted tumorigenesis. Our results suggest that CRKL has the ability to regulate colon cancer malignancy and CRKL has the potential to serve as a diagnosis and prognosis marker and a therapy target of colon cancer.

Colon Cancer Cells
Cell Growth
Invasion; Apoptosis
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