ArticleFrontiers in oncology2021
SQSTM1/p62 Promotes Cell Growth and Triggers Autophagy in Papillary Thyroid Cancer by Regulating the AKT/AMPK/mTOR Signaling Pathway.
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026Review
- Autophagy in thyroid cancer: stage-dependent switch, mutation-specific regulation, and therapeutic targeting.Oncology reviews · 2026Review
- p62 mRNA suppresses NLRP1 expression in cutaneous SCC cells through miR-34a-5p.Cell death & disease · 2025Article
- p62/SQSTM1 in cancer: phenomena, mechanisms, and regulation in DNA damage repair.Cancer metastasis reviews · 2025Review
- Article
- An investigation of the pattern and mechanism of comorbidity in patients with Hashimoto's thyroiditis.Frontiers in endocrinology · 2025Article
- Uncovering the connection between obesity and thyroid cancer: the therapeutic potential of adiponectin receptor agonist in the AdipoR2-ULK axis.Cell death & disease · 2024Article
- Proximity labeling reveals dynamic changes in the SQSTM1 protein network.bioRxiv : the preprint server for biology · 2024Article
- XTP8 Promotes Ovarian Cancer Progression by Activating AKT/AMPK/mTOR Pathway to Regulate EMT.Cell biochemistry and biophysics · 2024Article
- Drug repositioning in thyroid cancer: from point mutations to gene fusions.Frontiers in oncology · 2024Review
- PRKD3 promotes proliferation of liver cancer cells: a downstream proteomics profiling study.American journal of translational research · 2024Article
- The new insights into autophagy in thyroid cancer progression.Journal of translational medicine · 2023Review
- Mesenchymal stem cell-derived exosomes ameliorate TGF-β1-induced endometrial fibrosis by altering their miRNA profile.American journal of translational research · 2023Article
- High p62 expression suppresses the NLRP1 inflammasome and increases stress resistance in cutaneous SCC cells.Cell death & disease · 2022Article
- Non-Apoptotic Programmed Cell Death in Thyroid Diseases.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Identification of an Endoplasmic Reticulum Stress-Related Gene Signature to Evaluate the Immune Status and Predict the Prognosis of Hepatocellular Carcinoma.Frontiers in genetics · 2022Article
- A functional role for Serum Amyloid A in the molecular regulation of autophagy in breast cancer.Frontiers in oncology · 2022Article
- Article
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThyroid cancer is one of the most common endocrine malignancies worldwide, and papillary thyroid cancer (PTC) is the most common pathologic type of thyroid cancer. SQSTM1/p62 activity mediates different biological functions. This study aimed to investigate the effect of SQSTM1/p62, a multifunctional receptor, on biological function and autophagy characteristics in the human PTC cell line TPC-1.
methodsA total of 105 primary PTC samples and matched adjacent normal thyroid tissue samples were obtained to evaluate the expression of p62 in clinical patients. A similar p62 expression pattern was found in PTC cell lines and normal human thyroid follicular epithelial cells. To evaluate the effect of SQSTM1/p62 on TPC-1 cells, we constructed the p62 knockout cell line p62-KO-TPC-1. Cell proliferation, cell cycle, and cell apoptosis were analyzed by colony formation tests, Cell Counting Kit-8 (CCK-8) assays and flow cytometry
resultsOverall, p62 expression was higher in tumor tissues than in normal tissues in 73 of 105 PTC patients (69.5%). The expression level of p62 in the PTC cell line was higher than that in the normal thyroid cell line. Our data indicated that
conclusionsThe results indicate that p62 might mediate cell autophagy and apoptosis in TPC-1 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.