ArticleBMC cancer2016
Identification of SEC62 as a potential marker for 3q amplification and cellular migration in dysplastic cervical lesions.
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- ER stress as a trigger of UPR and ER-phagy in cancer growth and spread.Frontiers in oncology · 2022Pooled it
- Post-translational modifications of selective autophagy receptors: orchestrating cellular homeostasis, disease pathogenesis, and therapeutic opportunities.Cellular & molecular biology letters · 2026Review
- Unveiling ER-Phagy Receptors in Thyroid Cancer: A Combined Approach of Public Data Mining and In Vitro Validation.Clinical Medicine Insights. Oncology · 2026Article
- Article
- Selective autophagy in cancer: mechanisms, therapeutic implications, and future perspectives.Molecular cancer · 2024Review
- The 3q OncogeneInternational journal of molecular sciences · 2023Article
- Sec62 promotes gastric cancer metastasis through mediating UPR-induced autophagy activation.Cellular and molecular life sciences : CMLS · 2022Article
- Effect of the 3q26-coding oncogeneFrontiers in physiology · 2022Article
- The endoplasmic reticulum membrane protein Sec62 as potential therapeutic target inFrontiers in physiology · 2022Review
- Antagonizing Sec62 function in intracellular CaFrontiers in physiology · 2022Article
- Emerging View on the Molecular Functions of Sec62 and Sec63 in Protein Translocation.International journal of molecular sciences · 2021Review
- Advances in ER-Phagy and Its Diseases Relevance.Cells · 2021Review
- Complexity and Specificity of Sec61-Channelopathies: Human Diseases Affecting Gating of the Sec61 Complex.Cells · 2021Review
- Sec62 promotes stemness and chemoresistance of human colorectal cancer through activating Wnt/β-catenin pathway.Journal of experimental & clinical cancer research : CR · 2021Article
- Autophagy and organelle homeostasis in cancer.Developmental cell · 2021Review
- Expression ofCancers · 2021Article
- Article
- ER-phagy and human diseases.Cell death and differentiation · 2020Review
- Sec62 promotes early recurrence of hepatocellular carcinoma through activating integrinα/CAV1 signalling.Oncogenesis · 2019Article
- Expression of 3q oncogeneOncology letters · 2019Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChromosome 3 amplification affecting the 3q26 region is a common genomic alteration in cervical cancer, typically marking the transition of precancerous intraepithelial lesions to an invasive phenotype. Though potential 3q encoded target genes of this amplification have been identified, a functional correlation of potential oncogenic function is still missing. In this study, we investigated copy number changes and the expression level of SEC62 encoded at 3q26.2 as a new potential 3q oncogene in dysplastic cervical lesions and analyzed its role in cervical cancer cell biology.
methodsExpression levels of Sec62 and vimentin were analyzed in liquid based cytology specimens from 107 women with varying grades of cervical dysplasia ranging from normal cases to cancer by immunofluorescence cytology. Additionally, a subset of 20 representative cases was used for FISH analyses targeting SEC62. To further explore the functional role of Sec62 in cervical cancer, HeLa cells were transfected with a SEC62 plasmid or SEC62 siRNA and analyzed for their proliferation and migration potential using real-time monitoring and trans-well systems as well as changes in the expression of EMT markers.
resultsFISH analyses of the swabbed cells showed a rising number of SEC62 gains and amplifications correlating to the grade of dysplasia with the highest incidence in high grade squamous intraepithelial lesions and squamous cell carcinomas. When analyzing the expression level of Sec62 and vimentin, we found a gradually increasing expression level of both proteins according to the severity of the dysplasia. In functional analyses, SEC62 silencing inhibited and SEC62 overexpression stimulated the migration of HeLa cells with only marginal effects on cell proliferation, the expression level of EMT markers and the cytoskeleton structure.
conclusionsOur study suggests SEC62 as a target gene of 3q26 amplification and a stimulator of cellular migration in dysplastic cervical lesions. Hence, SEC62 could serve as a potential marker for 3q amplification, providing useful information about the dignity and biology of dysplastic cervical lesions.
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