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Related Concept Videos

The Ras Gene02:38

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Updated: May 9, 2025

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Polo-Like Kinase 1 Expression in Colorectal Cancer: Association With RAS Mutations.

Yasushi Tanaka1,2, Eiji Oki1, Ryota Nakanishi1

  • 1Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Cancer Science
|May 3, 2025
PubMed
Summary
This summary is machine-generated.

High Polo-like kinase 1 (PLK1) expression predicts poor outcomes in colorectal cancer (CRC) patients, especially those receiving adjuvant chemotherapy and with RAS mutations. Further research is needed to explore PLK1 as a prognostic biomarker.

Keywords:
RASadjuvant chemotherapycolorectal cancerpolo‐like kinase 1prognosis

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Biomarkers

Background:

  • Polo-like kinase 1 (PLK1) is crucial for cell division.
  • Its prognostic value in colorectal cancer (CRC), particularly with RAS mutations, is not well understood.
  • Understanding PLK1's role can improve CRC treatment strategies.

Purpose of the Study:

  • To investigate PLK1 expression as a predictive biomarker for treatment outcomes in colorectal cancer (CRC).
  • To analyze the correlation between PLK1 expression, clinicopathological factors, and survival in CRC patients.
  • To evaluate the influence of RAS mutations on prognosis in CRC.

Main Methods:

  • Retrospective analysis of 225 colorectal cancer (CRC) patients.
  • Assessed PLK1 expression levels.
  • Correlated PLK1 expression with clinicopathological factors, survival, and RAS mutation status.

Main Results:

  • PLK1 expression significantly correlated with histopathology and perineural invasion.
  • High PLK1 expression was associated with a trend towards worse relapse-free survival in all CRC patients and stage III patients.
  • In stage III CRC patients receiving adjuvant chemotherapy, high PLK1 expression was an independent poor prognostic factor for relapse-free survival.
  • Mutated RAS status significantly predicted a poorer prognosis compared to wild-type RAS.

Conclusions:

  • High PLK1 expression is linked to poor survival in colorectal cancer (CRC) patients undergoing adjuvant chemotherapy.
  • PLK1 may serve as a predictive biomarker for CRC treatment outcomes.
  • RAS mutation status is a significant prognostic factor in CRC, potentially interacting with PLK1 expression.