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Related Experiment Video

Updated: Jun 23, 2026

A Multiplexed Luciferase-based Screening Platform for Interrogating Cancer-associated Signal Transduction in Cultured Cells

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Published on: July 3, 2013

p27 Expression in Wild-Type KRAS Colon Cancer.

Sonja Marinović¹, Iva Paladin², Anita Škrtić³

¹Division of Molecular Medicine, Ruđer Bosković Institute, Zagreb, Croatia.

Journal of Cellular and Molecular Medicine

|June 22, 2026

Summary

In wild-type KRAS colorectal cancer (CRC), p27 (a cell cycle regulator) shifts to the cytoplasm, potentially driving tumor growth. This cytoplasmic shift, linked to WT KRAS expression, suggests a new therapeutic target for CRC progression.

Keywords:

miR‐221/222 KRAS V109G SNP colon adenocarcinoma p27

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A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

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Published on: July 6, 2017

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

P27 (a cyclin-dependent kinase inhibitor) acts as a tumor suppressor in the nucleus but can promote cancer when in the cytoplasm.
KRAS mutations cause p27 to move to the cytoplasm, but its role in wild-type (WT) KRAS colorectal cancer (CRC) is unknown.

Purpose of the Study:

To investigate p27 localization in WT KRAS CRC.
To explore the roles of miR-221/222 and the CDKN1B V109G polymorphism in CRC risk.

Main Methods:

Immunohistochemistry was used to analyze p27 expression and localization in 50 WT KRAS CRC tissues and adjacent normal tissues.
Correlations between p27 levels, WT KRAS expression, miR-221/222 expression, and the CDKN1B V109G polymorphism were assessed.

Main Results:

P27 was most abundant in the superficial layer of normal mucosa, with significantly lower levels in tumor centers.
WT KRAS tumors expressing KRAS showed increased p27 levels and predominantly cytoplasmic localization at the invasive front.
miR-221/222 expression and the CDKN1B V109G polymorphism were not associated with CRC risk or p27 levels.

Conclusions:

This study is the first to examine p27 localization in WT KRAS CRC.
WT KRAS expression is associated with cytoplasmic p27 localization, suggesting a mechanism for tumor progression via altered p27 function.