ArticleEndocrine2021
Involvement of HMGB1 in vemurafenib resistance in thyroid cancer cells harboring BRAF (V600E) mutation by regulating excessive autophagy.
Article in Endocrine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- USP7 promotes follicular thyroid carcinoma progression and sorafenib resistance by activating NEK2/ATG5-mediated autophagy.Histology and histopathology · 2026Article
- Autophagy in thyroid cancer: stage-dependent switch, mutation-specific regulation, and therapeutic targeting.Oncology reviews · 2026Review
- HMGB1 as Double-Edged Regulator of Cancer Therapy: Mechanistic Roles in Chemotherapy Resistance and Immunotherapy Response.OncoTargets and therapy · 2026Review
- HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025Review
- An overview of autophagy inhibition as a potential clinical strategy in cancer therapy.Molecular pharmacology · 2025Review
- CTHRC1 is associated withBiomolecules & biomedicine · 2024Article
- The Cytoprotective Role of Autophagy in Response to BRAF-Targeted Therapies.International journal of molecular sciences · 2023Review
- Mechanisms involved in the HMGB1 modulation of tumor multidrug resistance (Review).International journal of molecular medicine · 2023Article
- The new insights into autophagy in thyroid cancer progression.Journal of translational medicine · 2023Review
- Review
- The Histone Deacetylase Inhibitor ITF2357 (Givinostat) Targets Oncogenic BRAF in Melanoma Cells and Promotes a Switch from Pro-Survival Autophagy to Apoptosis.Biomedicines · 2022Article
- Translocated HMGB3 is involved in papillary thyroid cancer progression by activating cytoplasmic TLR3 and transmembrane TREM1.Cell cycle (Georgetown, Tex.)Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThyroid carcinoma is the most frequent endocrine malignancy with high occurrence of BRAFV600E mutations. Though targeted therapy by vemurafenib, a specific inhibitor for BRAFV600E, has achieved great advance in therapeutic landscape, resistance occurrence is still a clinical challenge. Here, we sought to elucidate the function of high mobility group box 1 (HMGB1) in vemurafenib resistance in thyroid cancer harboring BRAF mutation.
methodsThe expression of HMGB1 in BRAF-mutant BCPAP and BRAF-wild CAL-62 cells were determined by qRT-PCR and western. Then, BCPAP cells were transfected with recombinant HMGB1 plasmids, and vemurafenib-resistant BCPAP-R cells were treated with si-HMGB1. The efficacy of HMGB1 on vemurafenib resistance was evaluated by detecting cell viability, apoptosis, and caspase-3 activity. In addition, the involvement of autophagy pathway was investigated.
resultsLower expression of HMGB1 was observed in BRAF-mutant BCPAP cells that had high sensitivity to vemurafenib. Overexpression of HMGB1 attenuated BCPAP cell sensitivity to vemurafenib by increasing cell viability and decreasing cell apoptosis and caspase-3 activity. Intriguingly, higher expression of HMGB1 was confirmed in vemurafenib-resistant BCPAP-R cells. Moreover, knockdown of HMGB1 sensitized BCPAP-R cells to vemurafenib resistance. Mechanistically, vemurafenib exposure induced autophagy by enhancing LC3II, Beclin-1 expression, and reducing autophagy substrate p62 expression. Importantly, targeting HMGB1 suppressed vemurafenib-induced autophagy. Blocking autophagy pathway with its inhibitor 3-MA offset BCPAP-R cell resistance to vemurafenib.
conclusionsThese findings highlight that HMGB1-mediated autophagy may account for vemurafenib resistance in thyroid cancer harboring BRAF mutation, implying a promising approach to overcome vemurafenib resistance in vemurafenib-mutant thyroid carcinomas.
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