ArticleOncology research2025
ETV1 transcriptional manipulation of KIFC1 regulates the progression of pancreatic cancer.
Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Integrated bulk, single-cell and spatial transcriptomic analyses identify KIFC1 as a driver of malignant progression in lung adenocarcinoma.Molecular biology reports · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Kinesin-14 family protein 1 (KIFC1) is abnormally overexpressed in various cancers, and the transcription factor ETS variant 1 (ETV1) is an oncogenic transcription factor in tumors. The potential binding sites on the KIFC1 promoter by ETV1 were observed; however, no evidence supports that ETV1 targets KIFC1. Aims: This study aimed to investigate the relationship between KIFC1 and ETV1, and their effects and mechanisms in pancreatic cancer. Methods: Pan-cancer analysis of KIFC1 expression was performed in GEPIA2 database. KIFC1 expression levels were determined by immunohistochemistry (IHC) in our pancreatic cancer cohort. The correlation between KIFC1 expression and prognosis, tumor mutation burden, tumor purity, mismatch repair, and high-frequency tumor mutated genes was analyzed using a series of bioinformatic tools. ETV1 targeting of KIFC1 promoter transcription was determined using luciferase reporter assay. KIFC1 knockdown and ETV1 overexpression were used to determine the role of the ETV1/KIFC1 axis in cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of pancreatic cancer cells Result: KIFC1 expression was increased in clinical specimens and pancreatic cancer cell lines and positively correlated with tumor mutation burden, tumor purity, mismatch repair, and KRAS and TP53 mutations. High KIFC1 expression was significantly associated with poor prognosis. Knockdown of KIFC1 suppressed the proliferation, migration, and invasion of pancreatic cancer cells and tumor growth. ETV1 overexpression increased KIFC1 expression and affected KIFC1 transcription. ETV1 overexpression reversed the role of KIFC1 knockdown in inhibiting cell proliferation, invasion, migration, and EMT, as validated Conclusions: KIFC1 serves as a tumor activator in pancreatic cancer by promoting proliferation, migration, invasion, and tumor growth, which may be partly manipulated by ETV1.
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