ArticleMolecular therapy oncolytics2020
miR-16-5p/PDK4-Mediated Metabolic Reprogramming Is Involved in Chemoresistance of Cervical Cancer.
Article in Molecular therapy oncolytics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
The trial behind it
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Beyond Junk DNA: Emerging Roles of Non-Coding RNAs in Cancer and Therapeutic Innovation.Biomolecules · 2026Review
- Pathogenic Mechanisms in Cervical Cancer: Energy Metabolism, Hypoxia and Therapy.Life (Basel, Switzerland) · 2026Review
- Article
- Differentially Expressed Genes Associated with the Development of Cervical Cancer.International journal of molecular sciences · 2025Article
- Development and validation of a prognostic prediction model for gastric cancer based on lipophagy-related genes.Translational cancer research · 2025Article
- DNMBP-AS1/hsa-miR-30a-5p/PGC1α axis suppresses tumor progression of colorectal cancer by inhibiting PKM2-mediated Warburg effect and enhance anti-PD-1 therapy efficacy.Cell death discovery · 2025Article
- Oleanolic acid alleviates ovarian cancer by regulating the miR-122/PDK4 axis to induce autophagy and inhibit glycolysisFrontiers in oncology · 2025Article
- Dihydroartemisinin suppresses glioma growth by repressing ERRα-mediated mitochondrial biogenesis.Molecular and cellular biochemistry · 2024Article
- Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc Pathway.Cancer medicine · 2024Article
- Glucose metabolism reprogramming in gynecologic malignant tumors.Journal of Cancer · 2024Review
- High glucose promotes benign prostatic hyperplasia by downregulating PDK4 expression.Scientific reports · 2023Article
- ESRRG-PKM2 axis reprograms metabolism to suppress esophageal squamous carcinoma progression and enhance anti-PD-1 therapy efficacy.Journal of translational medicine · 2023Article
- Role of microRNAs in glycolysis in gynecological tumors (Review).International journal of oncology · 2023Review
- Gene expression profiling and FDG-PET radiomics uncover radiometabolic signatures associated with outcome in DLBCL.Blood advances · 2023Article
- Diagnostic significance of dysregulated miRNAs in T-cell malignancies and their metabolic roles.Frontiers in oncology · 2023Review
- Silencing of circ_002136 sensitizes gastric cancer to paclitaxel by targeting the miR-16-5p/HMGA1 axis.Open medicine (Warsaw, Poland) · 2023Article
- Silencing of lncRNA MIR31HG promotes nasopharyngeal carcinoma cell proliferation and inhibits apoptosis through suppressing the PI3K/AKT signaling pathway.Journal of clinical laboratory analysis · 2022Article
- Downregulation of hsa_circ_0000885 suppressed osteosarcoma metastasis and progression via regulating E2F3 expression and sponging miR-16-5p.Regenerative therapy · 2022Article
- A review on the role of mir-16-5p in the carcinogenesis.Cancer cell international · 2022Review
- [miR-16-5p regulates apoptosis and migration of drug-resistant breast cancer cells by targeting YWHAQ].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer is one of the most prevalent malignancies in women worldwide. Therefore, investigation about molecular pathogenesis and related therapy targets of cervical cancer is an emergency. The molecular mechanisms responsible for the chemoresistance of cervical cancer were investigated by the use of doxorubicin (Dox)-resistant HeLa/Dox and SiHa/Dox cells. Our data showed that chemoresistant cells exhibited significantly higher glucose consumption, lactate production rate, and ATP levels than that of their parental cells. Among metabolic and glycolytic related genes, the expression of PDK4 was upregulated in Dox-resistant cells. Knockdown of PDK4 can decrease glucose consumption, lactate production rate, and ATP levels and further sensitize resistant cervical cancer cells to Dox treatment. By screening microRNAs (miRNAs), which can regulate expression of PDK4, we found that miR-16-5p was downregulated in chemoresistant cells. Overexpression of miR-16-5p can decrease the expression of PDK4 and sensitize the resistant cells to Dox treatment. Xenograft models confirmed that knockdown of PDK4 can increase chemotherapy efficiency for
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.