Small regulatory polypeptide of amino acid response negatively relates to poor prognosis and controls hepatocellular carcinoma progression via regulating microRNA‐5581‐3p/human cardiolipin synthase 1

Yin, Jian; Liu, Qian; Chen, Chao; Liu, Wenxiang

doi:10.1002/jcp.28383

Cited by 11 publications

(10 citation statements)

References 35 publications

(56 reference statements)

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“…Available data showed that overexpression of miR-5581-3p promoted cellular activities in hepatocellular carcinoma by inhibiting cardiolipin synthase 1. 26 This study supplemented the knowledge regarding the physiological function of hsa-miR-5581-3p.…”

Section: F8 Is a Target Gene Of Hsa-mir-5581-3p And Hsa-mir-mentioning

confidence: 69%

Hsa-miR-5581-3p and hsa-miR-542-3p target the F8 gene in hemophilia A without F8 mutations

Meng

2021

Mediterr J Hematol Infect Dis

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Objective: This study aims at uncovering the effects of microRNAs (miRNAs) on F8 gene and FVIII protein in hemophilia A (HA). Methods: F8-targeting miRNAs were predicted by TargetScan, miRDB and starBase. MiRNAs predicted by at least two of the three databases were selected for further study, and their expressions in the blood of HA patients without F8 mutations and healthy controls were detected. Dual-luciferase reporter assay was performed to verify the binding between hsa-miR-5581-3p/hsa-miR-542-3p and F8. The regulation of F8 by hsa-miR-5581-3p/hsa-miR-542-3p was investigated in human umbilical vein endothelial cells (HUVECs) and lymphoblastoid cell line (LCL) that displayed endogenous expression of FVIII. qRT-PCR was used to detect the expressions of miRNAs and F8 gene, and Western blotting was conducted to measure the expression of FVIII protein. Results: A total of 43 F8-targeting miRNAs were predicted by at least two of the three databases. Among these miRNAs, hsa-miR-5581-3p and hsa-miR-542-3p were highly expressed in the blood of HA patients and have not been reported in previous studies of HA. Both hsa-miR-5581-3p and hsa-miR-542-3p could bind the 3’UTR of F8 mRNA. Upregulation of hsa-miR-5581-3p or hsa-miR-542-3p suppressed the expressions of F8 mRNA and FVIII protein in HUVECs and LCL cells. Conclusion: Hsa-miR-5581-3p and hsa-miR-542-3p target the F8 gene and suppress the expression of FVIII protein, which may contribute to the development of HA without F8 mutations.

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Section: F8 Is a Target Gene Of Hsa-mir-5581-3p And Hsa-mir-mentioning

confidence: 69%

Hsa-miR-5581-3p and hsa-miR-542-3p target the F8 gene in hemophilia A without F8 mutations

Meng

2021

Mediterr J Hematol Infect Dis

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“…Mechanistically, in HepG2 and Hep3B HCC cell lines, overexpression of long non-coding RNA LINC00961 was proportionally correlated with CRLS1 mRNA and protein overexpression, resulting in the inhibition of HCC progression (i.e., inhibition of cell proliferation, migration, and invasion in HCC cells). Both LINC00961 and CRLS1 protein expression were downregulated in patients' HCC tumors [41]. These studies suggest a tumor suppressor function for CRLS1 that is co-expressed with other tumor suppressor proteins.…”

Section: Cardiolipin Metabolismmentioning

confidence: 70%

“…More studies also propose the tumor suppressor activity of CRLS1 in HCC. It has been found that LINC00961, a novel long non-coding RNA which has been uncovered as a tumor suppressor in lung cancer and glioma, was downregulated in HCC tissues and cell lines (HepG2 and Hep3B) [41]. Mechanistically, in HepG2 and Hep3B HCC cell lines, overexpression of long non-coding RNA LINC00961 was proportionally correlated with CRLS1 mRNA and protein overexpression, resulting in the inhibition of HCC progression (i.e., inhibition of cell proliferation, migration, and invasion in HCC cells).…”

Section: Cardiolipin Metabolismmentioning

confidence: 99%

Cardiolipin, the Mitochondrial Signature Lipid: Implication in Cancer

Ahmadpour

Mahéo

Servais

et al. 2020

IJMS

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Cardiolipins (CLs) are specific phospholipids of the mitochondria composing about 20% of the inner mitochondria membrane (IMM) phospholipid mass. Dysregulation of CL metabolism has been observed in several types of cancer. In most cases, the evidence for a role for CL in cancer is merely correlative, suggestive, ambiguous, and cancer-type dependent. In addition, CLs could play a pivotal role in several mitochondrial functions/parameters such as bioenergetics, dynamics, mitophagy, and apoptosis, which are involved in key steps of cancer aggressiveness (i.e., migration/invasion and resistance to treatment). Therefore, this review focuses on studies suggesting that changes in CL content and/or composition, as well as CL metabolism enzyme levels, may be linked with the progression and the aggressiveness of some types of cancer. Finally, we also introduce the main mitochondrial function in which CL could play a pivotal role with a special focus on its implication in cancer development and therapy.

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“…We showed miR-5581-3p was a target of LINC00526 through bioinformatic analysis, luciferase activity assay, and RIP assay. miR-5581-3p was previously found to be negatively regulated by LINC00961 in hepatocellular carcinoma and thus affect cancer progression [12]. Subsequently, BEX1 was confirmed as a target of miR-5581-3p in glioma.…”

Section: Discussionmentioning

confidence: 94%

Long Noncoding RNA LINC00526 Represses Glioma Progression via Regulating miR-5581-3p/BEX1

Yan

et al. 2021

Journal of Oncology

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The roles of long noncoding RNAs (lncRNAs) in regulating glioma progression have been widely recognized in recent years. This work was to investigate the roles and associated mechanisms of LINC00526 in glioma progression. LINC00526 expression in glioma tissues and cells and their normal counterparts was measured with quantitative real-time polymerase chain reaction method. Functions of LINC00526 in glioma were investigated with in vitro experiments. Moreover, competitive RNA (ceRNA) theory was employed to understand mechanisms of action of LINC00526 in glioma. LINC00526 was found to be decreased in glioma tissues and cell lines compared with their normal counterparts. Silencing the expression of LINC00526 promotes, while forcing its expression, inhibits glioma cell growth and invasion. Mechanism analyses showed LINC00526 functions as a sponge for microRNA-5581-3p (miR-5581-3p) to regulate brain-expressed X-linked 1 (BEX1) expression and, in the end, affects glioma progression. Collectively, our study indicated LINC00526 serves as a tumor-suppressive lncRNA and directly regulates miR-5581-3p/BEX1 axis in glioma.

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Small regulatory polypeptide of amino acid response negatively relates to poor prognosis and controls hepatocellular carcinoma progression via regulating microRNA‐5581‐3p/human cardiolipin synthase 1

Cited by 11 publications

References 35 publications

Hsa-miR-5581-3p and hsa-miR-542-3p target the F8 gene in hemophilia A without F8 mutations

Hsa-miR-5581-3p and hsa-miR-542-3p target the F8 gene in hemophilia A without F8 mutations

Cardiolipin, the Mitochondrial Signature Lipid: Implication in Cancer

Long Noncoding RNA LINC00526 Represses Glioma Progression via Regulating miR-5581-3p/BEX1

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