AI Article Synopsis
- The study focuses on the role of miR-144 in increasing the sensitivity of anaplastic thyroid carcinoma (ATC) cells to cisplatin, a common chemotherapy drug.
- Researchers found that low levels of miR-144 in ATC cells led to increased autophagy and decreased apoptosis, but miR-144 can counteract this by inhibiting the protein TGF-α.
- In both lab tests and animal models, enhancing miR-144 expression improved cisplatin sensitivity and reduced tumor growth by targeting TGF-α, indicating a potential therapeutic role for miR-144 in treating ATC.
Article Abstract
Background: We 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.
Methods: Thyroid 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.
Results: MiR-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.
Conclusion: MiR-144 could inhibit autophagy of ATC cells by down-regulating TGF-α, enhancing the cisplatin-sensitivity of ATC cells.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5927701 | PMC |
| http://dx.doi.org/10.1080/15384047.2018.1433502 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Telocinobufagin suppresses malignant metastasis of undifferentiated thyroid carcinoma via modulation of the LARP1-mTOR pathway.
Kaohsiung J Med Sci
January 2025
Department of Neck Surgery, Sanming First Hospital Affiliated to Fujian Medical University, Sanming, China.
Metastasis is the trigger of death in anaplastic thyroid cancer (ATC) patients, yet the specific mechanisms at play are still largely enigmatic. While the involvement of LARP1 in the metastatic process of various cancers has been documented, there is a noticeable gap in the literature regarding its potential influence on ATC metastasis. Molecular studies probed LARP1 expression within ATC cells, with subsequent in vitro experiments examining the effects of LARP1 on ATC cell metastasis and the mTOR signaling cascade.
View Article and Find Full Text PDFPersistent pre-exhausted CD8+ T cells shape the tumor immune microenvironment in anaplastic thyroid cancer.
Endocr Relat Cancer
January 2025
X Zheng, Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Anaplastic Thyroid Cancer (ATC) is an aggressive form of cancer with poor prognosis, heavily influenced by its tumor immune microenvironment (TIME). Understanding the cellular and gene expression dynamics within the TIME is crucial for developing targeted therapies. This study analyzes the immune microenvironment of ATC and Papillary Thyroid Cancer (PTC) using single-cell RNA sequencing (scRNA-seq).
View Article and Find Full Text PDFMG149 suppresses anaplastic thyroid cancer progression by inhibition of lysine acetyltransferase KAT5-mediated c-Myc acetylation.
Bull Cancer
December 2024
Department of General Surgery, People's Hospital of Dongxihu District, Wuhan 430040, Hubei, China. Electronic address:
Background: Anaplastic thyroid cancer (ATC) is a highly lethal form of thyroid cancer. lysine acetyltransferase 5 (KAT5) has been found to promote ATC development via c-Myc stabilization by previous study. We thus designed experiments to confirm the anti-tumor effect of a KAT5 inhibitor (MG149) in ATC.
View Article and Find Full Text PDFZYG-12/Hook's dual role as a dynein adaptor for early endosomes and nuclei is regulated by alternative splicing of its cargo binding domain.
Mol Biol Cell
December 2024
i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal.
The microtubule motor cytoplasmic dynein-1 transports and positions various organelles, but the molecular basis of this functional diversity is not fully understood. Cargo adaptors of the Hook protein family recruit dynein to early endosomes (EE) in fungi and human cells by forming the FTS-Hook-FHIP (FHF) complex. By contrast, the Hook homolog ZYG-12 recruits dynein to the nuclear envelope (NE) in the meiotic gonad and mitotic early embryo by forming a Linker of Nucleoskeleton and Cytoskeleton (LINC) complex.
View Article and Find Full Text PDFTargeting CDK2 Confers Vulnerability to Lenvatinib Via Driving Senescence in Anaplastic Thyroid Cancer.
Adv Sci (Weinh)
December 2024
Department of Head and Neck Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, P. R. China.
Anaplastic thyroid cancer (ATC) is the most lethal tumor arising from thyroid follicular epithelium. Lenvatinib is an off-label use option for ATC patients in many countries but an approved prescription in Japan. However, lenvatinib resistance is a substantial clinical challenge.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!