ArticleCancer biology & therapy2018
Effects of miR-144 on the sensitivity of human anaplastic thyroid carcinoma cells to cisplatin by autophagy regulation.
Article in Cancer biology & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- The Changing Face ofFrontiers in surgery · 2020Pooled it
- Exosome-mediated metabolic reprogramming: effects on thyroid cancer progression and tumor microenvironment remodeling.Molecular cancer · 2025Review
- MicroRNA-mediated autophagy regulation in thyroid cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Combined detection of inflammatory proteins is beneficial for diagnosing the papillary thyroid carcinoma and nodular goiter.iMetaOmics · 2024Article
- Biomarkers in Thyroid Cancer: Emerging Opportunities from Non-Coding RNAs and Mitochondrial Space.International journal of molecular sciences · 2024Review
- MicroRNAs as the critical regulators of autophagy-mediated cisplatin response in tumor cells.Cancer cell international · 2023Review
- Regulatory miRNAs in cancer cell recovery from therapy exposure and its implications as a novel therapeutic strategy for preventing disease recurrence.The Enzymes · 2023Article
- Non-coding RNAs associated with autophagy and their regulatory role in cancer therapeutics.Molecular biology reports · 2022Review
- Non-coding RNAs associated with autophagy and their regulatory role in cancer therapeutics.Molecular biology reports · 2022Review
- Analysis on Value of Applying Serum miR-144 and miR-221 Levels in Diagnosing Atherosclerosis.Journal of healthcare engineering · 2022Article
- Poorly Differentiated and Anaplastic Thyroid Cancer: Insights into Genomics, Microenvironment and New Drugs.Cancers · 2021Review
- Review
- Genomic amplification of long noncoding RNA HOTAIRM1 drives anaplastic thyroid cancer progression via repressing miR-144 biogenesis.RNA biology · 2021Article
- Research Progress on the Functions and Mechanism of circRNA in Cisplatin Resistance in Tumors.Frontiers in pharmacology · 2021Review
- Review
- Long non-coding RNA MALAT1 activates autophagy and promotes cell proliferation by downregulating microRNA-204 expression in gastric cancer.Oncology letters · 2020Article
- MicroRNA-144: A novel biological marker and potential therapeutic target in human solid cancers.Journal of Cancer · 2020Review
- MicroRNA-524-5p suppresses the progression of papillary thyroid carcinoma cells via targeting on FOXE1 and ITGA3 in cell autophagy and cycling pathways.Journal of cellular physiology · 2019Article
- miR‑144 promotes the proliferation and differentiation of bone mesenchymal stem cells by downregulating the expression of SFRP1.Molecular medicine reports · 2019Article
- The Network of Non-coding RNAs in Cancer Drug Resistance.Frontiers in oncology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe investigated the influence of miR-144 on the cisplatin-sensitivity of anaplastic thyroid carcinoma (ATC) cells and explored the internal molecular mechanism of miR-144.
methodsThyroid cancer cells ARO, TPC1 and normal thyroid cells HT-ori3 were used in this research. Expressions of miR-144 and TGF-α were uncovered by western blot and qRT-PCR. Expressions of autophagy-related protein LC3 II and apoptosis-related protein Caspase-3 and PARP were explored by western blot and immunofluorescence. Cell viability was detected by MTT assay and apoptosis condition was revealed by flow cytometric analysis and TUNEL staining. Dual-luciferase reporter assay was employed to verify the target relationship. Tissue sections were detected by IHC. Xenograft assay was conducted to further verify conclusions in vivo.
resultsMiR-144, which was low expressed in ATC cells and tissues, could inhibit autophagy activation induced by cisplatin, enhancing the sensitivity of ATC cells to cisplatin, and promoting cell apoptosis. TGF-α was the target of miR-144 and was negatively regulated by it. MiR-144 could improve the sensitivity of ATC cells to cisplatin and inhibit tumor growth by suppressing TGF-α both in vitro and in vivo.
conclusionMiR-144 could inhibit autophagy of ATC cells by down-regulating TGF-α, enhancing the cisplatin-sensitivity of ATC cells.
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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.