Mitochondria-Related Core Genes and TF-miRNA-hub mrDEGs Network in Breast Cancer

Yan, Li-rong; Wang, Ang; Lv, Zhi; Yuan, Yuan; Xu, Qinying

doi:10.21203/rs.3.rs-84002/v1

Cited by 2 publications

(2 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…International Publisher identified a novel TF-miRNA-mRNA co-regulatory network in pulmonary large-cell neuroendocrine carcinoma [9]. Yan et al discovered mitochondriarelated core genes and TF-miRNA-hub mrDEGs network in breast cancer [10]. We unveiled that the expression of miR-338-3p was obviously reduced in osteosarcoma in accordance to bioinformatics methods.…”

Section: Ivyspringmentioning

confidence: 62%

KLF9 regulates miR-338-3p/NRCAM axis to block the progression of osteosarcoma cells

et al. 2022

View full text Add to dashboard Cite

Background: MiR-338-3p is revealed to serve as a tumor suppressor in several carcinomas. Whereas, the effect of miR-338-3p in the progression of osteosarcoma has not been explored. The aim of this paper was to analyze the functional influences of miR-338-3p on osteosarcoma progression and the potential mechanism. Methods: The expression of genes and miRNAs in osteosarcoma cells was assessed via western blotting or quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Osteosarcoma cellular proliferation was explored by MTT and EdU incorporation assay. Osteosarcoma cellular migratory and invasive capacity was explored by wound-healing and transwell assay. Bioinformatics approaches were adopted to predict target genes. The relationships between miR-338-3p and neuron-glial-related cell adhesion (NRCAM), between kruppel-like factor 9 (KLF9) and miR-338-3p were verified by dual-luciferase reporter assay. Results: We found that miR-338-3p was reduced in osteosarcoma and that higher expression of miR-338-3p suppressed proliferative, invasive and migratory ability of osteosarcoma cells. Furthermore, the result showed that overexpression of NRCAM could reduce the anti-tumor role of miR-338-3p in osteosarcoma cells. In addition, we found that overexpression of KLF9 could enhance the expression level of miR-338-3p in osteosarcoma cells. Conclusion:The KLF9/miR-338-3p/NRCAM axis played a significant role in regulating osteosarcoma progression, which may become a promising therapeutic method for osteosarcoma.

show abstract

Section: Ivyspringmentioning

confidence: 62%

KLF9 regulates miR-338-3p/NRCAM axis to block the progression of osteosarcoma cells

et al. 2022

View full text Add to dashboard Cite

show abstract

“…In another study, hsa-mir-218-5p was reduced in gastric cancer cells allowing metastatic behavior, which could be associated with an increase in PGC1A expression [ 62 ]. Moreover, “in silico” analysis four microRNAs mitochondrial sub-localization indicated that hsa-mir-218-5p is located in the mitochondria [ 63 ]. Taken together, this suggests that microRNA hsa-mir-218-5p may regulate PGC1Α in humans and indicates a possible regulatory function of hsa-mir-218-5p over mitochondrial homeostasis.…”

Section: Discussionmentioning

confidence: 99%

The MicroRNA miR-696 is regulated by SNARK and reduces mitochondrial activity in mouse skeletal muscle through Pgc1α inhibition

Queiroz

Lessard

Ouchida

et al. 2021

Molecular Metabolism

View full text Add to dashboard Cite

Objective MicroRNAs (miRNA) are known to regulate the expression of genes involved in several physiological processes including metabolism, mitochondrial biogenesis, proliferation, differentiation, and cell death. Methods Using “in silico” analyses, we identified 219 unique miRNAs that potentially bind to the 3′UTR region of a critical mitochondrial regulator, the peroxisome proliferator-activated receptor gamma coactivator (PGC) 1 alpha ( Pgc1α ). Of the 219 candidate miRNAs, miR-696 had one of the highest interactions at the 3′UTR of Pgc1α , suggesting that miR-696 may be involved in the regulation of Pgc1α . Results Consistent with this hypothesis, we found that miR-696 was highly expressed in the skeletal muscle of STZ-induced diabetic mice and chronic high-fat-fed mice. C2C12 muscle cells exposed to palmitic acid also exhibited a higher expression of miR-696 . This increased expression corresponded with a reduced expression of oxidative metabolism genes and reduced mitochondrial respiration. Importantly, reducing miR-696 reversed decreases in mitochondrial activity in response to palmitic acid. Using C2C12 cells treated with the AMP-activated protein kinase (AMPK) activator AICAR and skeletal muscle from AMPKα2 dominant-negative (DN) mice, we found that the signaling mechanism regulating miR-696 did not involve AMPK. In contrast, overexpression of SNF1-AMPK-related kinase (SNARK) in C2C12 cells increased miR-696 transcription while knockdown of SNARK significantly decreased miR-696 . Moreover, muscle-specific transgenic mice overexpressing SNARK exhibited a lower expression of Pgc1α , elevated levels of miR-696 , and reduced amounts of spontaneous activity. Conclusions Our findings demonstrate that metabolic stress increases miR-696 expression in skeletal muscle cells, which in turn inhibits Pgc1α , reducing mitochondrial function. SNARK plays a role in this process as a metabolic stress signaling molecule inducing the expression of miR-696 .

show abstract

Mitochondria-Related Core Genes and TF-miRNA-hub mrDEGs Network in Breast Cancer

Cited by 2 publications

References 25 publications

KLF9 regulates miR-338-3p/NRCAM axis to block the progression of osteosarcoma cells

KLF9 regulates miR-338-3p/NRCAM axis to block the progression of osteosarcoma cells

The MicroRNA miR-696 is regulated by SNARK and reduces mitochondrial activity in mouse skeletal muscle through Pgc1α inhibition

Contact Info

Product

Resources

About