ArticleJournal of bioenergetics and biomembranes2021
KIFC1 promotes aerobic glycolysis in endometrial cancer cells by regulating the c-myc pathway.
Article in Journal of bioenergetics and biomembranes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 22 citations in OpenAlex.
- Targeting the KIFC1-SRSF3-PKM Axis Suppresses Cervical Cancer Glycolysis and Enhances Radiosensitivity.Journal of cellular and molecular medicine · 2026Article
- The Clinical Significance of KIFs in Cervical and Endometrial Cancer: from Mechanisms to Biomarker and Therapeutic Potential.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Targeting KIFC1 to disrupt centrosome clustering and trigger anaphase catastrophe in small-cell lung cancer.JCI insight · 2026Article
- PMM2 interacts with TRIM28 to recruit E2F4 and promote KIFC3-mediated tumor glycolysis and colorectal cancer progression.Oncogene · 2026Article
- KIFC1 is Associated With Sarcomatoid Differentiation, Immune Response, and a Poor Prognosis in Clear Cell Renal Cell Carcinoma.Cancer medicine · 2026Article
- Regulation of Histone Emulsification by HPDL via LDHA/LDHB Promotes EC Cell Proliferation.Oncology research · 2026Article
- LTBP2 promotes meningioma progression by enhancing glycolysis via the PI3K/AKT/mTOR/c-Myc signaling pathway.Discover oncology · 2025Article
- Metabolic interplay between endometrial cancer and tumor-associated macrophages: lactate-induced M2 polarization enhances tumor progression.Journal of translational medicine · 2025Article
- KIFC1 Overexpression Promotes Pancreatic Carcinoma Progression via Stabilising BUB1B.Journal of cellular and molecular medicine · 2025Article
- USP25-driven KIFC1 regulates MYCBP expression and promotes the progression of cervical cancer.Cell death & disease · 2025Article
- Mechanism of PTPN18 for regulating the migration and invasion of endometrial cancer cells via the MYC/PI3K/AKT pathway.Histology and histopathology · 2025Article
- ETV1 transcriptional manipulation of KIFC1 regulates the progression of pancreatic cancer.Oncology research · 2025Article
- Breast cancer shares many epidemiological, lifestyle, and local hormonal and metabolic underpinnings with endometrial and ovarian cancer: a narrative review.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2025Review
- KIFC1 depends on TRIM37-mediated ubiquitination of PLK4 to promote centrosome amplification in endometrial cancer.Cell death discovery · 2024Article
- CDK1 promotes the phosphorylation of KIFC1 to regulate the tumorgenicity of endometrial carcinoma.Journal of gynecologic oncology · 2024Article
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- Identification of KIFC1 as an independent prognostic marker in renal clear cell carcinoma correlates with tumor proliferation and immune infiltration.Scientific reports · 2023Article
- The Role of Reprogrammed Glucose Metabolism in Cancer.Metabolites · 2023Review
- Glucose metabolic reprogramming and its therapeutic potential in obesity-associated endometrial cancer.Journal of translational medicine · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer (EC) is a common gynecological malignant tumor worldwide. It is imperative to study pathogenesis and therapeutic targets for improving the prognosis of EC. The present study aimed to explore the function and mechanism of kinesin family member C1 (KIFC1) in EC. EC tumor and adjacent normal tissues were collected from 68 pairs of patients. The expression of KIFC1 in tissues and EC cells was analyzed by immunohistochemistry, qRT-PCR or western blot. MTT assay was used to test the cell viability. Flow cytometry was used to determine apoptosis and the cell cycle. Glucose uptake, lactate production, ATP contents and lactate dehydrogenase (LDH) activity were evaluated by a glucose metabolism kit. The expression of HMGA1, c-myc and glycolytic genes was assessed using western blot or qRT-PCR. A mouse xenograft model was established in BALB/c mice to detect tumor growth in vivo. KIFC1 was significantly upregulated in EC tumor tissues compared to adjacent normal control tissues. The upregulated expression of KIFC1 was correlated with poor prognosis in patients. Lentiviral-mediated overexpression of KIFC1 observably enhanced cell viability and reduced the apoptotic rate of Ishikawa and HEC-1B cells. Cell cycle progression was also expedited in the KIFC1 vector group. Moreover, overexpression of KIFC1 elevated glucose uptake, lactate production, ATP contents and LDH activity. However, knockdown of KIFC1 by short hairpin RNA (shRNA) showed the reverse effect on cellular functions. In addition, the expression of c-myc, GLUT1, LDHA and HK2 was increased by the KIFC1 vector. Moreover, HMGA1 regulated the expression of c-myc and glycolytic genes. Upregulated HMGA1 could rescue the effect of KIFC1 knockdown on cellular functions and the expression of glycolytic genes. Finally, KIFC1 knockdown inhibits tumor growth in vivo. The upregulation of KIFC1 was correlated with poor prognosis in EC. KIFC1 promoted aerobic glycolysis in endometrial cancer cells by regulating the HMGA1/c-myc pathway. KIFC1 may be a potential target for the diagnosis and therapy of EC.
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