MAOA-mediated reprogramming of stromal fibroblasts promotes prostate tumorigenesis and cancer stemness

Li, Jingjing; Pu, Tianjie; Liu, Yin; Li, Qinlong; Liao, Chun-Peng; Wu, Bainan

doi:10.1038/s41388-020-1217-4

Cited by 31 publications

(25 citation statements)

References 50 publications

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“…IHC analysis of clinical and xenograft tumor samples was performed as described previously (Li et al, 2020) using antibodies against WLS, CHGA, Ki-67, cleaved caspase 3, CD34, CD56, p-PKCδ or p-ERK. Details on the antibodies for IHC, including RRIDs, are provided in Supplemental Table 2.…”

Section: Llmentioning

confidence: 99%

WLS-Wnt signaling promotes neuroendocrine prostate cancer

et al. 2021

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Section: Llmentioning

confidence: 99%

WLS-Wnt signaling promotes neuroendocrine prostate cancer

et al. 2021

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“…Inhibition of JAK2/STAT3 significantly suppresses IL-6-induced EMT, cell migration and invasion in HCC and pancreatic cancer ( 40 , 41 ). Furthermore, monoamine oxidase A promotes tumour cell proliferation via IL-6/STAT3 signalling ( 42 ). Lee et al ( 43 ) reported that monoamine oxidase A was downregulated as a result of IL-6/IL-6R/STAT3 signalling, and this may be attributed to Epstein-Barr virus infection in nasopharyngeal carcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

Silencing of ISLR inhibits tumour progression and glycolysis by inactivating the IL‑6/JAK/STAT3 pathway in non‑small cell lung cancer

Zhang¹,

Li²,

Yang³

2021

Int J Mol Med

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Lung cancer is the second most frequent cancer type in both men and women, and it is considered to be one of the major causes of cancer-related mortality worldwide. However, few biomarkers are currently available for the diagnosis of lung cancer. The aim of the present study was to investigate the function of the immunoglobulin superfamily containing leucine-rich repeat ( ISLR ) gene in non-small cell lung cancer (NSCLC) cells, and to elucidate the underlying molecular mechanism of its action. The current study analysed ISLR expression in NSCLC tumour and normal tissues using The Cancer Genome Atlas cohort datasets. ISLR expression in NSCLC cell lines was determined using reverse transcription-quantitative PCR. Cell Counting Kit-8, soft agar colony formation, wound healing, Transwell, flow cytometry and glycolysis assays were performed to determine the effects of ISLR silencing or overexpression on cells. The expression levels of the genes involved in epithelial-mesenchymal transition (EMT), apoptosis and glycolysis were evaluated via western blotting. Transfected cells were exposed to the pathway activator, IL-6, to validate the regulatory pathway. ISLR was overexpressed in NSCLC tissues and cell lines. Overall, patients with high ISLR expression had lower survival rates. In addition, small interfering RNA- ISLR inhibited the proliferation, EMT, migration, invasion and glycolysis of NSCLC cells, and promoted their apoptosis. ISLR overexpression had the opposite effect on tumour progression and glycolysis in NSCLC cells. Gene set enrichment analysis and western blotting results indicated that the IL-6/Janus kinase (JAK)/STAT3 pathway was enriched in ISLR -related NSCLC. Knockdown of ISLR inhibited IL-6-induced proliferation, invasion, migration and glycolysis in human NSCLC cells. In summary, ISLR silencing can inhibit tumour progression and glycolysis in NSCLC cells by activating the IL-6/JAK/STAT3 signalling pathway, which is a potential molecular target for NSCLC diagnosis and treatment.

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“…Interestingly, SDC1 and MAOA were not only DEGs but also host genes of DECs. Literature reported SDC1 can repress inflammatory cytokine expression in epithelial [ 51 ] and epithelial apoptosis [ 52 ]. MAOA was also reported to promote tumor cell proliferation [53].…”

Section: Discussionmentioning

confidence: 99%

Identification of Differentially Expressed circRNAs, miRNAs, and Genes in Patients Associated with Cartilaginous Endplate Degeneration

et al. 2021

BioMed Research International

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Background. Intervertebral disc degeneration (IDD) disease is a global challenge because of its predominant pathogenic factor in triggering low back pain, whereas cartilaginous endplate degeneration (CEPD) is the main cause of IDD. Accumulating evidence have indicated that the differentially expressed microRNAs (DEMs) and differentially expressed genes (DEGs) have been determined to be involved in multiple biological processes to mediate CEPD progression. However, the differentially expressed circular RNAs (DECs) and their potential biofunctions in CEPD have not been identified. Methods. GSE153761 dataset was analyzed using R software to predict DECs, DEMs, and DEGs. Pathway enrichment analysis of DEGs and host genes of DECs and protein-protein interaction network of DEGs were conducted to explore their potential biofunctions. Furthermore, we explore the potential relationship between DEGs and DECs. Results. There were 74 DECs, 17 DEMs, and 68 DEGs upregulated whereas 50 DECs, 16 DEMs, and 67 DEGs downregulated in CEPD group. Pathway analysis unveiled that these RNAs might regulate CEPD via mediating inflammatory response, ECM metabolism, chondrocytes apoptosis, and chondrocytes growth. A total of 17 overlapping genes were predicted between the host genes of DEGs and DECs, such as SDC1 and MAOA. Moreover, 6 upregulated DECs, of which hsa_circ_0052830 was the most upregulated circRNA in CEPD, were derived from the host genes SDC1, whereas 8 downregulated DECs were derived from the host genes MAOA. Conclusion. This will provide novel clues for future experimental studies to elucidate the pathomechanism of CEPD and therapeutic targets for CEPD-related diseases.

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MAOA-mediated reprogramming of stromal fibroblasts promotes prostate tumorigenesis and cancer stemness

Cited by 31 publications

References 50 publications

WLS-Wnt signaling promotes neuroendocrine prostate cancer

WLS-Wnt signaling promotes neuroendocrine prostate cancer

Silencing of ISLR inhibits tumour progression and glycolysis by inactivating the IL‑6/JAK/STAT3 pathway in non‑small cell lung cancer

Identification of Differentially Expressed circRNAs, miRNAs, and Genes in Patients Associated with Cartilaginous Endplate Degeneration

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