دورية أكاديمية

LINC00998‐encoded micropeptide SMIM30 promotes the G1/S transition of cell cycle by regulating cytosolic calcium level

التفاصيل البيبلوغرافية
العنوان: LINC00998‐encoded micropeptide SMIM30 promotes the G1/S transition of cell cycle by regulating cytosolic calcium level
المؤلفون: Jin‐E Yang, Wang‐Jing Zhong, Jin‐Feng Li, Ying‐Ying Lin, Feng‐Ting Liu, Hao Tian, Ya‐Jing Chen, Xiao‐Yu Luo, Shi‐Mei Zhuang
المصدر: Molecular Oncology, Vol 17, Iss 5, Pp 901-916 (2023)
بيانات النشر: Wiley, 2023.
سنة النشر: 2023
المجموعة: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
مصطلحات موضوعية: cell cycle, G1/S transition, micropeptide, SMIM30, sORF, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
الوصف: The biological functions of short open reading frame (sORF)‐encoded micropeptides remain largely unknown. Here, we report that LINC00998, a previously annotated lncRNA, was upregulated in multiple cancer types and the sORF on LINC00998 encoded a micropeptide named SMIM30. SMIM30 was localized in the membranes of the endoplasmic reticulum (ER) and mitochondria. Silencing SMIM30 inhibited the proliferation of hepatoma cells in vitro and suppressed the growth of tumor xenografts and N‐nitrosodiethylamine‐induced hepatoma. Overexpression of the 5′UTR‐sORF sequence of LINC00998, encoding wild‐type SMIM30, enhanced tumor cell growth, but this was abolished when a premature stop codon was introduced into the sORF via single‐base deletion. Gain‐ and loss‐of‐function studies revealed that SMIM30 peptide but not LINC00998 reduced cytosolic calcium level, increased CDK4, cyclin E2, phosphorylated‐Rb and E2F1, and promoted the G1/S phase transition and cell proliferation. The effect of SMIM30 silencing was attenuated by a calcium chelator or the agonist of sarco/endoplasmic reticulum calcium ATPase (SERCA) pump. These findings suggest a novel function of micropeptide SMIM30 in promoting G1/S transition and cell proliferation by enhancing SERCA activity and reducing cytosolic calcium level.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1878-0261
1574-7891
Relation: https://doaj.org/toc/1574-7891; https://doaj.org/toc/1878-0261
DOI: 10.1002/1878-0261.13358
URL الوصول: https://doaj.org/article/b9d2b14013b34f4c8dd53497ee48dc0c
رقم الأكسشن: edsdoj.b9d2b14013b34f4c8dd53497ee48dc0c
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:18780261
15747891
DOI:10.1002/1878-0261.13358