Tumor Biology

, Volume 37, Issue 7, pp 8841–8848 | Cite as

Investigation of FIH-1 and SOCS3 expression in KRAS mutant and wild-type patients with colorectal cancer

  • Ladan Vakil
  • Reza Najafipour
  • Nasser Rakhshani
  • Farhad Zamani
  • Arman Morakabati
  • Amir Javadi
Original Article


Colorectal cancer (CRC) is a multistep process based on the accumulation of somatic mutations in genes such as APC and KRAS. Data on the presence of mutations in KRAS gene in CRC and its relationship with clinicopathological parameters and expression of genes involved in tumor progression are scarce. We unbiasedly examined the KRAS status in samples from 99 patients and its correlation with clinicopathological parameters such as age, sex, tumor location, lymph node metastasis, tumor stage, tumor grade, and vascular invasion. Consistent with reports of other researchers, 38.4 % of our samples harbored KRAS mutation in their genomes with preferential mutation in codon 12 (89.4 %). Nevertheless, unlike previous reports, we were not able to correlate KRAS status with clinicopathological parameters (P > 0.05) except for vascular invasion. Patients with KRAS mutation have more vascular invasion compared with patient having wild-type KRAS. Next, we investigated the expression of two tumor suppressor genes, factor-inhibiting hypoxia-inducible factor 1 (FIH-1) and suppressor of cytokine signaling (SOCS3), in both KRAS mutant and wild-type groups and looked for any correlation between their expression and clinicopathological parameters. Although the expression of both genes was not regular, none of the clinicopathological parameters were associated with the expressions of FIH-1 and SOCS3 at mRNA level (P > 0.05). However, decline in FIH-1 expression at protein level in KRAS mutant group was correlated with stage IV and grade 2 of tumor (P ≤ 0.05). Our results demonstrated that there is no or low correlation between KRAS status, FIH-1, and SOCS3 expression with epidemiologic and clinicpathological characteristics in CRC.


Colorectal cancer KRAS mutation FIH-1 and SOCS3 



This project has been funded by Qazvin University of Medical Sciences and Iran University of Medical Sciences. The authors also thank Mehran Ghaderi and Farhad Ghoujeghi for their experimental advices.

Compliance with ethical standards

Conflicts of interest



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Copyright information

© International Society of Oncology and BioMarkers (ISOBM) 2016

Authors and Affiliations

  • Ladan Vakil
    • 1
    • 2
    • 3
  • Reza Najafipour
    • 1
    • 2
  • Nasser Rakhshani
    • 3
  • Farhad Zamani
    • 3
  • Arman Morakabati
    • 4
  • Amir Javadi
    • 5
  1. 1.Department of Molecular Medicine, School of MedicineQazvin University of Medical SciencesQazvinIran
  2. 2.Cellular and Molecular Research CenterQazvin University of Medical SciencesQazvinIran
  3. 3.GI and Liver Disease Research Center, Firoozgar HospitalIran University of Medical SciencesTehranIran
  4. 4.Molecular Pathology Department of Mehr General HospitalTehranIran
  5. 5.Departments of Medical Informatics, School of Allied Medical SciencesTehran University of Medical SciencesTehranIran

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