The role of monoamine oxidase A in HPV-16 E7-induced epithelial-mesenchymal transition and HIF-1α protein accumulation in non-small cell lung cancer cells

Huang, Bingyu; Zhou, Zhiyuan; Liu, Jiao; Wu, Xin; Li, Xiangyong; He, Qing; Zhang, Peihua; Tang, Xudong

doi:10.7150/ijbs.46966

Cited by 23 publications

(26 citation statements)

References 51 publications

(78 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tang's group found positive expression of MAOA in 9 out of 12 LUAD tumors by IHC ( 18 ). Recently, we reported that MAOA plays a critical role in NSLC migration and HPV-16 E7 induced-HIF-1α protein accumulation in NSCLC cells ( 17 ). Another group found that a potential inhibitor of MAOA, G11, increases the sensitivity of chemotherapy drug and metastasis of NSCLC cells ( 19 ).…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, we showed that MAOA abrogates cancer cell growth and serves as an independent biomarker for LUAD. Monoamine oxidase A was reported to be an oncogene in NSCLC (17,37). Tang's group found positive expression of MAOA in 9 out of 12 LUAD tumors by IHC (18).…”

Section: Discussionmentioning

confidence: 99%

“…Clinical and in vitro data indicate that MAOA functions as a tumor suppressor in hepatocellular carcinoma ( 11 ), cholangiocarcinoma ( 12 ), pheochromocytoma ( 13 ), neuroblastoma ( 14 ), renal cell carcinoma ( 15 ), and oral and pharyngeal cancers ( 16 ). MAOA is overexpressed in NSCLC and stimulates the epithelial–mesenchymal transition in cancer cells ( 17 , 18 ). An inhibitor of MAOA repressed paclitaxel-resistant NSCLC metastasis and growth ( 19 ).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Monoamine Oxidase A Inhibits Lung Adenocarcinoma Cell Proliferation by Abrogating Aerobic Glycolysis

et al. 2021

View full text Add to dashboard Cite

Lung adenocarcinoma (LUAD) accounts for ~30% of all lung cancers and is one of the causes of cancer-related death worldwide. As the role of monoamine oxidase A (MAOA) in LUAD remains unclear, in this study, we examine how MAOA affects LUAD cell proliferation. Analyses of both public data and our data reveal that the expression of MAOA is downregulated in LUAD compared with non-tumor tissue. In addition, the expression of MAOA in tumors correlates with clinicopathologic features, and the expression of MAOA serves as an independent biomarker in LUAD. In addition, the overexpression of MAOA inhibits LUAD cell proliferation by inducing G1 arrest in vitro. Further mechanistic studies show that MAOA abrogates aerobic glycolysis in LUAD cells by decreasing hexokinase 2 (HK2). Finally, the expression of HK2 shows a negative correlation with MAOA in LUAD, and high HK2 predicts poor clinical outcome. In conclusion, our findings indicate that MAOA functions as a tumor suppressor in LUAD. Our results indicate that the MAOA/HK2 axis could be potential targets in LUAD therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Monoamine Oxidase A Inhibits Lung Adenocarcinoma Cell Proliferation by Abrogating Aerobic Glycolysis

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Moreover, these changes were more obvious in the 1% oxygen concentration group than in the 5% oxygen concentration group in both LUSC and LUAD cells. is may be because, under hypoxic conditions, the transcriptional instability of tumor cells may cause the activation of some cancer survival-related factors, resulting in the enhancement of tumor migration and invasion and promotion of cancer development [25,26].…”

Section: Discussionmentioning

confidence: 99%

Alternatively Expressed Transcripts Analysis of Non-Small Cell Lung Cancer Cells under Different Hypoxic Microenvironment

Wang

et al. 2021

Journal of Oncology

View full text Add to dashboard Cite

Globally, non-small cell lung cancer (NSCLC) is the most fatal form of malignancy. Numerous studies have shown that people living at high altitudes are at a higher risk for cancer. Hypoxia is one of the most important features in high altitude area. Compared with normal cells, cancer cells are more adapted to hypoxia atmosphere. However, at high altitudes, hypoxic conditions are also accompanied by other altered environmental conditions. To identify the single influence of hypoxia, we performed second-generation sequencing to identify gene expression changes triggered by the different oxygen concentrations. We identified 782 genes in A549 cells and 1122 genes in H520 cells that showed altered expression by the combined analysis in 5% oxygen concentration group and 1% oxygen concentration group control group. We further analyzed these targets and found 113 genes altered in both cell lines. Interestingly, we found KxD1 was the only one in both top 10 lists. Further analysis revealed KxD1 to be significantly elevated in NSCLC patients and negatively correlated with prognosis in stage I and II NSCLC patients. Moreover, this correlation reversed in stage III patients. Additionally, compared with patients who only received clean margin operation or chemotherapy, patients who received radiotherapy also showed opposite result. Thus, KxD1 may be a promising target for the treatment of NSCLC in high-altitude areas.

show abstract

“…Given the fact that MAOA was reported as a key regulator of epithelial-to-mesenchymal transition (EMT) in multiple cancers [20], we herein also wondered whether PCa bone metastasis could be inhibited by targeting MAOA induced EMT. By detection of the expression of EMT markers, we found that in PC3-378OE cells treated with GW4869, the expression of E-cad was signi cantly upregulated along with a signi cant downregulation of N-cad and vimintin expression (Fig.…”

Section: Overexpression Of Mir-378a-3p Inhibits Epithelial-tomesenchymal Transition (Emt) For Metastasis By Targeting Maoamentioning

confidence: 99%

Tumor-Derived miR-378a-3p-Containing Extracellular Vesicles Promote Osteolysis by Activating a Dyrk1a/Nfatc1/Angptl2 Axis for Bone Metastasis

Wang

et al. 2021

Preprint

View full text Add to dashboard Cite

Background The majority of the deaths of prostate cancer (PCa) are caused by progression to bone metastatic PCa. The importance of extracellular vesicles (EVs) in the formation of the pre-metastatic niche has been demonstrated in recent years. However, whether and how tumor-derived EVs interact with bone marrow macrophages (BMMs) to release EV-delivered microRNAs to promote osteolysis and to activate pre-metastatic niche formation for PCa bone metastasis remain unclear. Methods Bioinformatics and qRT-PCR analyses were used to screen microRNAs and to identify the elevated expression of miR-378a-3p in both serum-derived EVs from PCa patients and in culture medium-derived EVs from PCa cell lines. Functional assays in vitro and in vivo were performed to investigate the functions of miR-378a-3p during PCa progression. IF staining and Dual-luciferase reporter, co-IP, western blot, RIP and ChIP assays were conducted to reveal the underlying mechanism. Results We found that EV-mediated release of miR-378a-3p from tumor cells was upregulated in bone-metastatic PCa which keeps a low intracellular concentration of miR-378a-3p, to promote proliferation and the MAOA-mediated epithelial-to-mesenchymal transition (EMT) in PCa cells. In addition, we demonstrated that the enrichment of miR-378a-3p in tumor derived EVs was induced by overexpression of hnRNPA2B1 as a transfer chaperone. After miR-378a-3p-enriched EVs were taken in by BMMs, elevated intracellular concentration of miR-378a-3p promoted osteolytic progression by targeting the Dyrk1a/Nfatc1 pathway. Mechanistically, inhibition of Dyrk1a by miR-378a-3p improved the nuclear translocation of Nfatc1 to promote expression of the downstream target gene Angptl2. As a feedback, increased secretion of Angptl2 into the tumor environment promoted PCa progression. Conclusions Our findings indicate that tumor-derived miR-378a-3p-containing EVs play a significant role in promoting prostate cancer bone metastasis by activating a Dyrk1a/Nfatc1/Angptl2 axis in BMMs to induce osteolytic progression, which implicates that miR-378a-3p may be a potential predictor of metastatic PCa. Moreover, reducing the release of miR-378a-3p-containing EVs or inhibiting the recruitment of miR-378a-3p into tumor-derived EVs might be a potential therapeutic strategy for PCa metastasis.

show abstract

The role of monoamine oxidase A in HPV-16 E7-induced epithelial-mesenchymal transition and HIF-1α protein accumulation in non-small cell lung cancer cells

Cited by 23 publications

References 51 publications

Monoamine Oxidase A Inhibits Lung Adenocarcinoma Cell Proliferation by Abrogating Aerobic Glycolysis

Monoamine Oxidase A Inhibits Lung Adenocarcinoma Cell Proliferation by Abrogating Aerobic Glycolysis

Alternatively Expressed Transcripts Analysis of Non-Small Cell Lung Cancer Cells under Different Hypoxic Microenvironment

Tumor-Derived miR-378a-3p-Containing Extracellular Vesicles Promote Osteolysis by Activating a Dyrk1a/Nfatc1/Angptl2 Axis for Bone Metastasis

Contact Info

Product

Resources

About