Jin Lingli, Chen Danxiang, Hirachan Suzita, Bhandari Adheesh, Huang Qidi
Department of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR China, 325000.
Department of Surgery, Breast Unit, Tribhuvan University Teaching Hospital, Kathmandu, Nepal.
J Cancer. 2022 Jan 1;13(3):831-846. doi: 10.7150/jca.65879. eCollection 2022.
Breast cancer is a common malignant tumor for women and its incidence has increased constantly in recent decades. The underlying molecular means of breast tumorigenesis endure uncertain. With the sequencing expertise, we found that the SEC61G gene is overexpressed in tumor tissues. However, the biological function of SEC61G in breast malignancy has yet to be determined. We investigated the SEC61G expression level, genetic alteration, IHC, immune infiltration, diagnostic value, survival analysis, and functional enrichment analysis by bioinformatics analysis. Then, experiments were done. We investigated that SEC61G was greater in breast cancer tissues related to adjacent non-tumor tissues through qRT-PCR. We performed proliferation, colony formation, migration, invasion assays, and EMT-related phenotype to determine the specific biological functions of SEC61G in breast cancer cell lines (MDA-MB-231, BT-549) transfected with small interfering RNA. SEC61G expression and exon expression were higher in the tumor while the level of SEC61G methylation was higher in normal tissues. The expression level of SEC61G was connected with immune infiltration and survival and was an effective diagnostic and prognostic indicator. The functional enrichment analysis of SEC61G prompted that SEC61G might play a tumor-promoting role via the EMT pathway. experiments indicated that knocking down SEC61G considerably impaired the colony formation, cck-8, migration, and invasion, and induced apoptosis of the breast cancer cell lines. The experiments also indicated that ectopic expression of SEC61G could influence EMT. This study revealed that SEC61G plays vital tumorigenic functions and acts as a novel oncogene in breast cancer.
乳腺癌是女性常见的恶性肿瘤，近几十年来其发病率持续上升。乳腺肿瘤发生的潜在分子机制尚不清楚。通过测序技术，我们发现SEC61G基因在肿瘤组织中过表达。然而，SEC61G在乳腺恶性肿瘤中的生物学功能尚未确定。我们通过生物信息学分析研究了SEC61G的表达水平、基因改变、免疫组化、免疫浸润、诊断价值、生存分析和功能富集分析。然后，进行了实验。通过qRT-PCR，我们研究发现乳腺癌组织中SEC61G的表达高于相邻的非肿瘤组织。我们进行了增殖、集落形成、迁移、侵袭实验以及与上皮-间质转化（EMT）相关的表型分析，以确定SEC61G在转染了小干扰RNA的乳腺癌细胞系（MDA-MB-231、BT-549）中的具体生物学功能。SEC61G的表达和外显子表达在肿瘤中较高，而SEC61G的甲基化水平在正常组织中较高。SEC61G的表达水平与免疫浸润和生存相关，是一个有效的诊断和预后指标。SEC61G的功能富集分析提示SEC61G可能通过EMT途径发挥促肿瘤作用。实验表明，敲低SEC61G会显著损害乳腺癌细胞系的集落形成、cck-8、迁移和侵袭能力，并诱导其凋亡。实验还表明，SEC61G的异位表达可影响EMT。本研究揭示了SEC61G在乳腺癌中发挥着至关重要的致瘤功能，并作为一种新型癌基因起作用。
