Journal
JOURNAL OF PERSONALIZED MEDICINE
Volume 11, Issue 12, Pages -Publisher
MDPI
DOI: 10.3390/jpm11121361
Keywords
breast cancer; kinesin family member C1 (KIFC1; HSET); centrosome amplification; neoplastic progression; tumorigenesis; human mammary epithelial cells (HMECs); high risk; cellular senescence; basal-like
Funding
- City of Hope Comprehensive Cancer Center Biomarker Core [CA220693, CA24619]
Ask authors/readers for more resources
The transformation and progression of pre-invasive breast lesions is a poorly understood enigma, with no current radiologic or molecular biomarkers available to successfully stratify high-risk lesions. The Kinesin family member C1 (KIFC1/HSET) may play a key role in enabling pre-neoplastic cells to bypass senescence barriers necessary for malignant transformation, and further research could potentially identify it as a risk-stratifying biomarker.
The enigma of why some premalignant or pre-invasive breast lesions transform and progress while others do not remains poorly understood. Currently, no radiologic or molecular biomarkers exist in the clinic that can successfully risk-stratify high-risk lesions for malignant transformation or tumor progression as well as serve as a minimally cytotoxic actionable target for at-risk subpopulations. Breast carcinogenesis involves a series of key molecular deregulatory events that prompt normal cells to bypass tumor-suppressive senescence barriers. Kinesin family member C1 (KIFC1/HSET), which confers survival of cancer cells burdened with extra centrosomes, has been observed in premalignant and pre-invasive lesions, and its expression has been shown to correlate with increasing neoplastic progression. Additionally, KIFC1 has been associated with aggressive breast tumor molecular subtypes, such as basal-like and triple-negative breast cancers. However, the role of KIFC1 in malignant transformation and its potential as a predictive biomarker of neoplastic progression remain elusive. Herein, we review compelling evidence suggesting the involvement of KIFC1 in enabling pre-neoplastic cells to bypass senescence barriers necessary to become immortalized and malignant. We also discuss evidence inferring that KIFC1 levels may be higher in premalignant lesions with a greater inclination to transform and acquire aggressive tumor intrinsic subtypes. Collectively, this evidence provides a strong impetus for further investigation into KIFC1 as a potential risk-stratifying biomarker and minimally cytotoxic actionable target for high-risk patient subpopulations.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available