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Targeting RAS signaling pathway as a potential therapeutic target in the treatment of colorectal cancer
Author(s) -
Bahrami Afsane,
Hassanian Seyed Mahdi,
ShahidSales Soodabeh,
Farjami Zahra,
Hasanzadeh Malihe,
Anvari Kazem,
Aledavood Amir,
Maftouh Mina,
Ferns Gordon A.,
Khazaei Majid,
Avan Amir
Publication year - 2018
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25890
Subject(s) - kras , cetuximab , neuroblastoma ras viral oncogene homolog , colorectal cancer , medicine , cancer research , pi3k/akt/mtor pathway , mapk/erk pathway , viral oncogene , cancer , targeted therapy , carcinogenesis , oncogene , oncology , signal transduction , biology , cell cycle , genetics
The V‐Ki‐ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) is frequently dysregulated in colorectal cancer (CRC). It is involved in the modulation of several downstream effectors, that include: Raf/Mek/Erk, PI3K/Akt, RalGDS/p38MAPK, and Rac/Rho, and thereby influences tumorigenesis, the invasive behaviors of tumor cell, and resistance to therapy. There is growing evidence exploring the use of drugs that target these pathways in the treatment of CRC. Cetuximab has been approved for CRC patients without a KRAS mutation, or for EGFR‐expressing metastatic CRC, although some of the patients have a mutation of KRAS and NRAS. This review summarizes the recent knowledge about the therapeutic potential of targeting RAS with particular emphasis on recent preclinical and clinical studies in treatment of CRC.