<scp>microRNA</scp>‐100 functions as a tumor suppressor in non‐small cell lung cancer via regulating epithelial‐mesenchymal transition and Wnt/β‐catenin by targeting <scp>HOXA1</scp>

Han, Weizhong; Ren, Xiaoxia; Yang, Yupeng; Li, Haixia; Zhao, Lin; Zx, Lin

doi:10.1111/1759-7714.13459

Cited by 20 publications

(16 citation statements)

References 40 publications

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“…HOXA1 encodes a DNA-binding transcription factor that regulates gene expression, morphogenesis, and differentiation. Previous studies have reported that HOXA1 contributes to cancer pathogenesis and progression, immunosuppressive activity of myeloid-derived suppressor cells, and therapeutic response ( 54 – 60 ). The results of the rescue assays indicated that LINC00958 promotes lung cancer progression by regulating the transcriptional activity of HOXA1.…”

Section: Discussionmentioning

confidence: 99%

MYC/MAX-Activated LINC00958 Promotes Lung Adenocarcinoma by Oncogenic Transcriptional Reprogramming Through HOXA1 Activation

Zhang

et al. 2022

Front. Oncol.

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BackgroundLung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer. The role of the long non-coding RNA (lncRNA) LINC00958, which regulates the malignant behavior of multiple tumors, in LUAD has not been elucidated.MethodsTissue microarray, FISH, and qRT-PCR were used to detect the expression of LINC00958. Plasmid and viral infections were used to manipulate gene expression. The role of LINC00958 in LUAD was studied by cell proliferation analysis, cell apoptosis analysis, cell migration and invasion analysis, and subcutaneous inoculation of animal models. At the same time, RNA-Seq, RNA pull-down, ChIRP, ChIP, and luciferase reporter gene assays were performed to clarify the mechanism.ResultsThe expression of LINC00958 in LUAD tissues was significantly upregulated when compared with that in adjacent tissues and could independently predict poor survival of patients with LUAD. LINC00958 knockdown significantly inhibited the growth and metastasis of lung cancer cells in vitro and in vivo. LINC00958 localized to the nucleus, regulated oncogenes and metabolism-related and immune response-related genes, and interacted with histones. The targets of LINC00958 were TRPV3, STAP2, and EDN2 promoters with motifs of HOXA1, NANOG, FOSL2, JUN, and ATF4. Moreover, HOXA1 overexpression mitigated the LINC00958 knockdown-induced oncogenic phenotype. MYC/MAX motif, which was detected at the cis-element of LINC00958, trans-activated the LINC00958 promoter.ConclusionsMYC/MAX-trans-activated LINC00958 promotes the malignant behavior of LUAD by recruiting HOXA1 and inducing oncogenic reprogramming.

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Section: Discussionmentioning

confidence: 99%

MYC/MAX-Activated LINC00958 Promotes Lung Adenocarcinoma by Oncogenic Transcriptional Reprogramming Through HOXA1 Activation

Zhang

et al. 2022

Front. Oncol.

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“…Next, we identified significant downregulation of miR-100-5p in the BALF-derived exosomes from COPD patients as compared to healthy smokers. Functionally, miR-100 is linked to the regulation of epithelial–mesenchymal transition (EMT), apoptosis, and inflammation [ 51 , 52 ]. Furthermore, Akbas and colleagues have demonstrated downregulation of miR-100-5p in the serum of COPD patients when compared to healthy smokers, which is in accordance with our study results [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

Distinct Exosomal miRNA Profiles from BALF and Lung Tissue of COPD and IPF Patients

Kaur

Maremanda

Campos

et al. 2021

IJMS

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Chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) are chronic, progressive lung ailments that are characterized by distinct pathologies. Early detection biomarkers and disease mechanisms for these debilitating diseases are lacking. Extracellular vesicles (EVs), including exosomes, are small, lipid-bound vesicles attributed to carry proteins, lipids, and RNA molecules to facilitate cell-to-cell communication under normal and diseased conditions. Exosomal miRNAs have been studied in relation to many diseases. However, there is little to no knowledge regarding the miRNA population of bronchoalveolar lavage fluid (BALF) or the lung-tissue-derived exosomes in COPD and IPF. Here, we determined and compared the miRNA profiles of BALF- and lung-tissue-derived exosomes of healthy non-smokers, smokers, and patients with COPD or IPF in independent cohorts. Results: Exosome characterization using NanoSight particle tracking and TEM demonstrated that the BALF-derived exosomes were ~89.85 nm in size with a yield of ~2.95 × 1010 particles/mL in concentration. Lung-derived exosomes were larger in size (~146.04 nm) with a higher yield of ~2.38 × 1011 particles/mL. NGS results identified three differentially expressed miRNAs in the BALF, while there was one in the lung-derived exosomes from COPD patients as compared to healthy non-smokers. Of these, miR-122-5p was three- or five-fold downregulated among the lung-tissue-derived exosomes of COPD patients as compared to healthy non-smokers and smokers, respectively. Interestingly, there were a large number (55) of differentially expressed miRNAs in the lung-tissue-derived exosomes of IPF patients compared to non-smoking controls. Conclusions: Overall, we identified lung-specific miRNAs associated with chronic lung diseases that can serve as potential biomarkers or therapeutic targets.

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“…Next, we identified significant downregulation of miR-100-5p in the BALF-derived exosomes from COPD patients as compared to healthy smokers. Functionally, miR-100 has been linked to the regulation of epithelial-mesenchymal transition (EMT), apoptosis and inflammation (54, 55). Furthermore, Akbas and colleagues have demonstrated downregulation of miR-100-5p in the serum of COPD patients when compared to healthy smokers, which is in accordance to our study results (56).…”

Section: Discussionmentioning

confidence: 99%

Distinct exosomal miRNA profiles from BALF and lung tissue from COPD and IPF patients

Kaur

Maremanda

Campos

et al. 2021

Preprint

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BackgroundChronic Obstructive Pulmonary Disease (COPD) and Idiopathic Pulmonary Fibrosis (IPF) are chronic, progressive lung ailments which are characterized by distinct pathologies. Early detection biomarkers and disease mechanisms for these debilitating diseases are lacking. Exosomes are small extracellular vesicles attributed to carry proteins, mRNA, miRNA and sncRNA to facilitate cell-to-cell communication under normal and diseased conditions. Exosomal miRNAs have been studied in relation to many diseases. However, there is little to no knowledge regarding the miRNA population of BALF or the lung tissue derived exosomes in COPD and IPF. Here, we determined and compared the miRNA profiles of BALF and lung tissue-derived exosomes from healthy non-smokers, healthy smokers, and patients with COPD and IPF in independent cohorts.ResultsExosome characterization using NanoSight particle tracking and TEM demonstrated that the BALF-derived exosomes were approximately 89.85 nm in size and ∼2.95 × 1010 particles/mL. Lung-derived exosomes were ∼146.04 nm in size and ∼2.38 × 1011 particles/mL. NGS results identified three differentially expressed miRNAs in the BALF, while one in the lung-derived exosomes from COPD patients as compared to healthy non-smokers. Of these, three- and five-fold downregulation of miR-122-5p amongst the lung tissue-derived exosomes from COPD patients as compared to healthy non-smokers and smokers, respectively. Interestingly, there were key 55 differentially expressed miRNAs in the lung tissue-derived exosomes of IPF patients compared to non-smoking controls.ConclusionsOverall, we identified specific miRNAs to develop as biomarkers or targets for pathogenesis of these chronic lung diseases.

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microRNA‐100 functions as a tumor suppressor in non‐small cell lung cancer via regulating epithelial‐mesenchymal transition and Wnt/β‐catenin by targeting HOXA1

Cited by 20 publications

References 40 publications

MYC/MAX-Activated LINC00958 Promotes Lung Adenocarcinoma by Oncogenic Transcriptional Reprogramming Through HOXA1 Activation

MYC/MAX-Activated LINC00958 Promotes Lung Adenocarcinoma by Oncogenic Transcriptional Reprogramming Through HOXA1 Activation

Distinct Exosomal miRNA Profiles from BALF and Lung Tissue of COPD and IPF Patients

Distinct exosomal miRNA profiles from BALF and lung tissue from COPD and IPF patients

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