Reduced expression of miR-30c-5p promotes hepatocellular carcinoma progression by targeting RAB32

He, Zheng; Tian, Meng; Fu, Xuan

doi:10.1016/j.omtn.2021.08.033

Cited by 12 publications

(8 citation statements)

References 34 publications

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“…In the present study, it was demonstrated that TNF-α treatment significantly decreased the miR-30c-5p expression level in RAOECs. Previous studies have indicated that miR-30 family members, especially miR-30c-5p, act as protective factors in numerous solid tumors, such as non-small cell lung ( 39 ), pancreatic ( 40 ) and liver ( 41 ) tumors. Recently, miR-30c-5p has been reported to be closely associated with the development of cardiovascular diseases, including AS ( 19 ), diabetic nephropathy ( 42 ) and myocardial ischemia-reperfusion injury ( 43 ).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of the long non‑coding RNA MALAT1 ameliorates TNF‑α‑mediated endothelial cell pyroptosis via the miR‑30c‑5p/Cx43 axis

et al. 2023

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Long noncoding RNAs (lncRNAs) are related to the development of atherosclerosis (AS). However, the role of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in tumor necrosis factor-α (TNF-α)-induced rat aortic endothelial cell (RAOEC) pyroptosis, as well as the underlying mechanisms, remain unclear. RAOEC morphology was assessed using an inverted microscope. The mRNA and/or protein expression levels of MALAT1, microRNA(miR)-30c-5p and connexin 43 (Cx43) were assessed using reverse transcription-quantitative PCR (RT-qPCR) and/or western blotting, respectively. The relationships among these molecules were validated by dual-luciferase reporter assays. Biological functions, such as LDH release, pyroptosis-associated protein levels and the proportion of PI-positive cells, were evaluated using a LDH assay kit, western blotting and Hoechst 33342/PI staining, respectively. The present study demonstrated that compared with the control group, the mRNA expression levels of MALAT1 and protein expression levels of Cx43 were significantly up-regulated, whereas miR-30c-5p mRNA expressions levels were significantly decreased in TNF-α-treated RAOEC pyroptosis. Knockdown of MALAT1 or Cx43 significantly attenuated the increase in LDH release, pyroptosis-associated protein expression and PI-positive cell numbers among RAOEC treated using TNF-α, whereas an miR-30c-5p mimic exerted the opposite effect. Furthermore, miR-30c-5p was demonstrated to be a negative regulator of MALAT1 and could also target Cx43. Finally, co-transfection with siMALAT1 and miR-30c-5p inhibitor could attenuate the protective effect of MALAT1 knockdown against TNF-α-mediated RAOEC pyroptosis by upregulation of Cx43 expression. In conclusion, MALAT1 might serve an important role in TNF-α-mediated RAOEC pyroptosis by regulating the miR-30c-5p/Cx43 axis, which would provide a potential novel diagnostic and therapeutic target for AS.

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Section: Discussionmentioning

confidence: 99%

Knockdown of the long non‑coding RNA MALAT1 ameliorates TNF‑α‑mediated endothelial cell pyroptosis via the miR‑30c‑5p/Cx43 axis

et al. 2023

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“…Therefore, elucidating the main regulators and signaling pathways of malignant glioma in ltration, especially the mesenchymal transition and tumor aggression, is expected to improve GBM therapeutic outcomes. The role of Rab32 in tumors is poorly explored, with only few studies reporting that Rab32 promotes tumor progression in hepatocellular and ovarian cancers (20,34), but no study of Rab32 is performed on glioma. Here, we are the rst to address the mesenchymal transition and cell invasion roles of Rab32 in GBM.…”

Section: Discussionmentioning

confidence: 99%

“…Rab32 belongs to the Ras-like small GTPase superfamily, which regulate membrane dynamics, including membrane fusion/ ssion, exocytosis, and cytoskeletal tra cking (18,19). A recent study showed that Rab32 serves as an oncogene in hepatocellular carcinoma with the potential to promote the growth and invasion of tumor cells, while a higher level of Rab32 was strongly related to the advanced tumor stage and poor survival in patients with hepatocellular carcinoma (20). However, the role of Rab32 in GBM, as well as its underlying subcellular and molecular mechanisms remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Rab32 promotes glioblastoma migration and invasion via regulation of ERK/Drp1-mediated mitochondrial fission

Chen

et al. 2022

Preprint

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Background and objective: The highly widespread and infiltrative nature of glioblastoma multiforme (GBM) makes complete surgical resection hard, causing high recurrence rate and poor patients’ prognosis. However, the mechanism underlying GBM migration and invasion is still unclear. In this study, we investigated the role of a Ras-related protein Rab32 on GBM and uncovered its underlying molecular and subcellular mechanisms that contributed to GBM aggressiveness. Method: The correlation of Rab32 expression with patient prognosis and tumor grade was investigated by public dataset analysis and clinical specimen validation. The effect of Rab32 on migration and invasion of GBM had been evaluated using wound healing assay, cell invasion assay, as well as protein analysis upon Rab32 manipulations. Mitochondrial dynamics of cells upon Rab32 alterations were detected by immunofluorescence staining and western blotting. Both the subcutaneous and intracranial xenograft tumor model were utilized to evaluate the effect of Rab32 on GBM in vivo. Results: The expression level of Rab32 is significantly elevated in the GBM, especially in the most malignant mesenchymal subtype, and is positively correlated with tumor pathological grade and poor prognosis. Knockdown of Rab32 attenuated the capability of GBM’s migration and invasion. It also suppressed the expression levels of invasion-related proteins (MMP2 and MMP9) as well as mesenchymal transition markers (N-cadherin, vimentin). Interestingly, Rab32 transported Drp1 to mitochondrial from the cytoplasm and modulated mitochondrial fission in an ERK1/2 signaling-dependent manner. Furthermore, silencing of Rab32 in vivo suppressed tumor malignancy via ERK/Drp1 axis. Conclusion: Rab32 regulates ERK1/2/Drp1-dependent mitochondrial fission and causes mesenchymal transition, promoting migration and invasion of GBM. It serves as a novel therapeutic target for GBM, especially for the most malignant mesenchymal subtype.

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“…Rab32 belongs to the Ras-like small GTPase superfamily, which regulate membrane dynamics, including membrane fusion/fission, exocytosis, and cytoskeletal trafficking [18,19]. A recent study showed that Rab32 serves as an oncogene in hepatocellular carcinoma with the potential to promote the growth and invasion of tumor cells, while a higher level of Rab32 was strongly related to the advanced tumor stage and poor survival in patients with hepatocellular carcinoma [20]. However, the role of Rab32 in GBM, as well as its underlying subcellular and molecular mechanisms remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Rab32 promotes glioblastoma migration and invasion via regulation of ERK/Drp1-mediated mitochondrial fission

Chen

et al. 2023

Cell Death Dis

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The highly widespread and infiltrative nature of glioblastoma multiforme (GBM) makes complete surgical resection hard, causing high recurrence rate and poor patients’ prognosis. However, the mechanism underlying GBM migration and invasion is still unclear. In this study, we investigated the role of a Ras-related protein Rab32 on GBM and uncovered its underlying molecular and subcellular mechanisms that contributed to GBM aggressiveness. The correlation of Rab32 expression with patient prognosis and tumor grade was investigated by public dataset analysis and clinical specimen validation. The effect of Rab32 on migration and invasion of GBM had been evaluated using wound healing assay, cell invasion assay, as well as protein analysis upon Rab32 manipulations. Mitochondrial dynamics of cells upon Rab32 alterations were detected by immunofluorescence staining and western blotting. Both the subcutaneous and intracranial xenograft tumor model were utilized to evaluate the effect of Rab32 on GBM in vivo. The expression level of Rab32 is significantly elevated in the GBM, especially in the most malignant mesenchymal subtype, and is positively correlated with tumor pathological grade and poor prognosis. Knockdown of Rab32 attenuated the capability of GBM’s migration and invasion. It also suppressed the expression levels of invasion-related proteins (MMP2 and MMP9) as well as mesenchymal transition markers (N-cadherin, vimentin). Interestingly, Rab32 transported Drp1 to mitochondrial from the cytoplasm and modulated mitochondrial fission in an ERK1/2 signaling-dependent manner. Furthermore, silencing of Rab32 in vivo suppressed tumor malignancy via ERK/Drp1 axis. Rab32 regulates ERK1/2/Drp1-dependent mitochondrial fission and causes mesenchymal transition, promoting migration and invasion of GBM. It serves as a novel therapeutic target for GBM, especially for the most malignant mesenchymal subtype.

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Reduced expression of miR-30c-5p promotes hepatocellular carcinoma progression by targeting RAB32

Cited by 12 publications

References 34 publications

Knockdown of the long non‑coding RNA MALAT1 ameliorates TNF‑α‑mediated endothelial cell pyroptosis via the miR‑30c‑5p/Cx43 axis

Knockdown of the long non‑coding RNA MALAT1 ameliorates TNF‑α‑mediated endothelial cell pyroptosis via the miR‑30c‑5p/Cx43 axis

Rab32 promotes glioblastoma migration and invasion via regulation of ERK/Drp1-mediated mitochondrial fission

Rab32 promotes glioblastoma migration and invasion via regulation of ERK/Drp1-mediated mitochondrial fission

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