LINC00092 Modulates Oxidative Stress and Glycolysis of Breast Cancer Cells via Pyruvate Carboxylase-Mediated AKT/mTOR Pathway

Abstract

Background. The discovery of noncoding RNAs (ncRNAs) offers new options for cancer-targeted therapy. This study is aimed at exploring the regulatory function of LINC00092 on breast cancer (BC) oxidative stress and glycolysis, along with internal mechanism concerning pyruvate carboxylase (PC). Methods. Bioinformatics analysis was used to explore LINC00092 (or friend leukemia virus integration 1 (FLI1)) expression on BC progression, as well as oxidative stress and glycolysis in BC. After LINC00092 overexpression or silence, BC cell viability, proliferation, migration, invasion, oxidative stress, glycolysis, and AKT/mTOR pathway were detected. Following 2-DG, SC79, or MK2206 treatment, effects of LINC00092 on BC cells were measured. Moreover, regulatory activity of LINC00092 in PC expression was analyzed. Whether PC participated in the modulation of LINC00092 on BC cell functions was explored. Results. LINC00092 was lowly expressed in BC and negatively related to BC progression. FLI1 bound to LINC00092 promoter to positively modulate LINC00092. LINC00092 overexpression inhibited BC cell proliferation, migration, invasion, oxidative stress, glycolysis, and AKT/mTOR pathway and likewise suppressed BC growth in vivo. Silence of LINC00092 had opposite influences. 2-DG partially reversed the LINC00092 silence-resulted increase of BC cell proliferation. SC79 alleviated the function of LINC00092 overexpression on BC cell functions. MK2206 had the contrary influence of SC79. Besides, LINC00092 bound to PC to modulate ubiquitination degradation of PC protein. PC took part in the influences of LINC00092 on BC cell functions. Conclusions. LINC0092 modulates oxidative stress and glycolysis of BC cells via the PC-mediated AKT/mTOR pathway, which is possibly a target for BC diagnosis and therapy.

tRF-1:30-Gly-CCC-3 inhibits thyroid cancer via binding to PC and modulating metabolic reprogramming

“…It has been confirmed in previous research that PC expression is dysregulated in several tumor types, including lung cancer, breast cancer, PTC ( Wang et al, 2021 ; Liu et al, 2022b ; Chen et al, 2022 ), etc. As shown in Fig 4A , PC was significantly elevated in PTC tissues.…”

“…mechanisms by which tRFs in cancer cells bind protein partners and affect posttranscriptional regulation. The LINC00092 has been reported to interact with PC to modulate glycolysis and oxidative stress of breast cancer cells, a novel biological mechanism by which noncoding RNA association with PC regulates cancer metabolism (Chen et al, 2022). To elucidate whether tRF-30 can mediate the metabolic mechanism of PTC via its interaction with PC, we performed LC-MS-based on metabolite levels in BCPAP cells.…”

Long noncoding RNAs: glycolysis regulators in gynaecologic cancers

“…LINC00092 is a gene with no functional annotations and is found in the intergenic regions of 9q22.32. Linc00092 has been found as a glycolysis-related lncRNA in breast cancer cells and cardiac fibroblast [173,174]. Zhao and his colleagues discovered that LINC00092 functions in OC cell proliferation and metastasis via cancer-associated fibroblasts (CAFs).…”

Retracted: LINC00092 Modulates Oxidative Stress and Glycolysis of Breast Cancer Cells via Pyruvate Carboxylase-Mediated AKT/mTOR Pathway

“…This article has been retracted by Hindawi, as publisher, following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of systematic manipulation of the publication and peer-review process.…”