Decreased expression of microRNA-320a promotes proliferation and invasion of non-small cell lung cancer cells by increasing VDAC1 expression

Zhang, Guanxin; Jiang, Gengxi; Wang, Chong; Zhong, Keng; Zhang, Jiajun; Xue, Qing; Li, Xin; Jin, Hai; Li, Bailing

doi:10.18632/oncotarget.9943

Cited by 55 publications

(40 citation statements)

References 33 publications

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“…Additionally, when 3′ UTR of VDAC1 was cloned downstream of luciferase gene in pMIR vector, mimic miR‐320a efficiently decreased the luciferase activity thereby confirming post‐transcriptional regulation of VDAC1 transcripts via miR‐320a. Recently, miR320a‐mediated regulation of VDAC1 was indicated in cervical cancer and non‐small cell lung cancer (NSCLC) (Li et al, ; Zhang et al, ), which is also in agreement with our findings.…”

Section: Discussionsupporting

confidence: 93%

Novel insights into role of miR-320a-VDAC1 axis in astrocyte-mediated neuronal damage in neuroAIDS

Fatima

Prajapati

Saleem

et al. 2016

Glia

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Astroglia are indispensable component of the tripartite synapse ensheathing innumerous soma and synapses. Its proximity to neurons aids the regulation of neuronal functions, health and survival through dynamic neuroglia crosstalk. Susceptibility of astrocyte to HIV-1 infection and subsequent latency culminates in compromised neuronal health. The viral protein HIV-1 transactivator of transcription (Tat) is neurotoxic. HIV-1 Tat is detected in brain of AIDS patients even in cases where viral load is non-detectable due to successful HAART therapy. Recently, we demonstrated that HIV-1 Tat triggers excess ATP release from astrocytes that causes neuronal death by activating purinergic receptor system. Using well-characterized model system of human primary astrocytes and neurons, we probed into the molecular mechanism for enhanced ATP release in HIV-1 Tat affected astrocytes. HIV-1 Tat modulated the miRNA machinery in astrocytes and perturbed the levels of voltage dependent anion channel 1 (VDAC1), a channel present in the outer mitochondrial membrane and plasma membrane that regulates extracellular ATP release. Our studies with autopsy tissue sections also showed concordantly dysregulated VDAC1 and miR-320a levels in HIV-1 patients suffering from mild cognitive impairment (MCI). We report a novel molecular cascade of miRNA-mediated ATP release through regulation of VDAC1. Downregulation of VDAC1 either with miR-320a mimic or VDAC1 siRNA in HIV-1 Tat-affected astroglia could rescue the neurons from glia-mediated indirect death. Our findings reveal a novel upstream therapeutic target that could be employed to thwart the astroglia-mediated neurotoxicity in HIV-1 neuropathogenesis. GLIA 2017;65:250-263.

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Section: Discussionsupporting

confidence: 93%

Novel insights into role of miR-320a-VDAC1 axis in astrocyte-mediated neuronal damage in neuroAIDS

Fatima

Prajapati

Saleem

et al. 2016

Glia

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“…Mir‐320a is de‐regulated in several cancer types such as gastric, breast, colon and lung cancer . Recent works demonstrated the role of mir‐320a as tumor suppressor in NSCLC by directly regulating IGF‐1R or VDAC1 expression suggesting this miRNA as a potential therapeutic target. Furthermore, mir‐320a was also involved in lung metastasis formation through down‐regulation of STAT3 and NRP‐1 .…”

Section: Discussionmentioning

confidence: 99%

Circulating mir‐320a promotes immunosuppressive macrophages M2 phenotype associated with lung cancer risk

Fortunato

Borzi

Milione

et al. 2019

Intl Journal of Cancer

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miRNAs play a central role in the complex signaling network of cancer cells with the tumor microenvironment. Little is known on the origin of circulating miRNAs and their relationship with the tumor microenvironment in lung cancer. Here, we focused on the cellular source and relative contribution of different cell types to circulating miRNAs composing our risk classifier of lung cancer using in vitro/in vivo models and clinical samples. A cell‐type specific expression pattern and topography of several miRNAs such as mir‐145 in fibroblasts, mir‐126 in endothelial cells, mir‐133a in skeletal muscle cells was observed in normal and lung cancer tissues. Granulocytes and platelets are the major contributors of miRNAs release in blood. miRNAs modulation observed in plasma of lung cancer subjects was consistent with de‐regulation of the same miRNAs observed during immunosuppressive conversion of immune cells. In particular, activated neutrophils showed a miRNA profile mirroring that observed in plasma of lung cancer subjects. Interestingly mir‐320a secreted by neutrophils of high‐risk heavy‐smokers promoted an M2‐like protumorigenic phenotype through downregulation of STAT4 when shuttled into macrophages. These findings suggest a multifactorial and nonepithelial cell‐autonomous origin of circulating miRNAs associated with risk of lung cancer and that circulating miRNAs may act in paracrine signaling with causative role in lung carcinogenesis and immunosuppression.

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“…Additionally, miR-320a has been observed to be an independent prognostic factor where decreased miR-320a expression is correlated with lower survival in invasive breast cancer. [32] The anti-proliferative and tumor-suppressing effects of miR-320a have also been recorded in lung cancer [33], prostate cancer [34], gastric cancer [35], leukemia [36, 37], and nasopharyngeal carcinoma [38]. …”

Section: Discussionmentioning

confidence: 99%

Identification of MicroRNAs as Breast Cancer Prognosis Markers through the Cancer Genome Atlas

et al. 2016

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Breast cancer is the second-most common cancer and second-leading cause of cancer mortality in American women. The dysregulation of microRNAs (miRNAs) plays a key role in almost all cancers, including breast cancer. We comprehensively analyzed miRNA expression, global gene expression, and patient survival from the Cancer Genomes Atlas (TCGA) to identify clinically relevant miRNAs and their potential gene targets in breast tumors. In our analysis, we found that increased expression of 12 mature miRNAs—hsa-miR-320a, hsa-miR-361-5p, hsa-miR-103a-3p, hsa-miR-21-5p, hsa-miR-374b-5p, hsa-miR-140-3p, hsa-miR-25-3p, hsa-miR-651-5p, hsa-miR-200c-3p, hsa-miR-30a-5p, hsa-miR-30c-5p, and hsa-let-7i-5p —each predicted improved breast cancer survival. Of the 12 miRNAs, miR-320a, miR-361-5p, miR-21-5p, miR-103a-3p were selected for further analysis. By correlating global gene expression with miRNA expression and then employing miRNA target prediction analysis, we suggest that the four miRNAs may exert protective phenotypes by targeting breast oncogenes that contribute to patient survival. We propose that miR-320a targets the survival-associated genes RAD51, RRP1B, and TDG; miR-361-5p targets ARCN1; and miR-21-5p targets MSH2, RMND5A, STAG2, and UBE2D3. The results of our stringent bioinformatics approach for identifying clinically relevant miRNAs and their targets indicate that miR-320a, miR-361-5p, and miR-21-5p may contribute to breast cancer survival.

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Decreased expression of microRNA-320a promotes proliferation and invasion of non-small cell lung cancer cells by increasing VDAC1 expression

Cited by 55 publications

References 33 publications

Novel insights into role of miR-320a-VDAC1 axis in astrocyte-mediated neuronal damage in neuroAIDS

Novel insights into role of miR-320a-VDAC1 axis in astrocyte-mediated neuronal damage in neuroAIDS

Circulating mir‐320a promotes immunosuppressive macrophages M2 phenotype associated with lung cancer risk

Identification of MicroRNAs as Breast Cancer Prognosis Markers through the Cancer Genome Atlas

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