Recent advances in searching c-Myc transcriptional cofactors during tumorigenesis

Caforio, Matteo; Socolovschi, Cristina; Iacovelli, Stefano; Fanciulli, Maurizio; Locatelli, Franco; Folgiero, Valentina

doi:10.1186/s13046-018-0912-2

Cited by 44 publications

(41 citation statements)

References 71 publications

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“…To further explore the molecular mechanism of miRNA-145 suppressing PD-L1 expression, we carried out a bioinformatics analysis on potential target genes that could be directly regulated by miR-145 and a transcription factor, c-Myc, was found to be one of its potential target genes. As a member of the Myc family, c-Myc controls stability and transcriptional activity of target gene via binding DNA on heterodimerization with Myc-associated factor X [38]. We confirmed the direct regulatory effect of miR-145 on c-Myc using luciferase reporter gene detection.…”

Section: Discussionsupporting

confidence: 63%

Cisplatin-mediated down-regulation of miR-145 contributes to up-regulation of PD-L1 via the c-Myc transcription factor in cisplatin-resistant ovarian carcinoma cells

Sheng

Zhang

Wang

et al. 2019

Clinical and Experimental Immunology

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Summary Immune tolerance is one of the leading causes of chemotherapy resistance in carcinoma cases. Studies have shown that programmed cell death ligand‐1 (PD‐L1), an inhibitory molecule expressed by cancer cells, plays a significant role in immune tolerance through the induction of T cell dysfunction. The results of our RNA sequencing in previous studies revealed that microRNA‐145 (miR‐145), which is known to be down‐regulated by cisplatin in cisplatin‐resistant ovarian cancer cells, also represses gene PD‐L1 expression. However, the mechanism by which miR‐145 contributes to regulate PD‐L1 expression in cisplatin resistance of ovarian cancer is yet to be fully understood. Here, we show that cisplatin‐mediated miR‐145 down‐regulation increased PD‐L1 expression via targeting the c‐Myc transcription factor, thereby inducing T cell apoptosis in vitro. We also report that expression of miR‐145 is negatively correlated with PD‐L1 expression in human ovarian cancer tissues, malignant grades and the recurrent risks of ovarian cancer after chemotherapy. In summary, our findings suggest that the miR‐145/c‐Myc/PD‐L1 axis contributes to cisplatin resistance in ovarian cancer and support that miR‐145 might act as an adjuvant therapeutic target in chemotherapy of ovarian cancer.

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Section: Discussionsupporting

confidence: 63%

Cisplatin-mediated down-regulation of miR-145 contributes to up-regulation of PD-L1 via the c-Myc transcription factor in cisplatin-resistant ovarian carcinoma cells

Sheng

Zhang

Wang

et al. 2019

Clinical and Experimental Immunology

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“…FAM83A gene is located on chromosome 8q24 [23]. This region is known to contain the oncogene Myc, which is frequently amplified in cancer [24]. It has also been recently proved that long non-coding RNA (lncRNA) FAM83A-AS1 promotes lung adenocarcinoma by increasing FAM83A expression [25].…”

Section: Discussionmentioning

confidence: 99%

FAM83A is amplified and promotes tumorigenicity in non-small cell lung cancer via ERK and PI3K/Akt/mTOR pathways

Hu¹,

Wang²,

Wang³

et al. 2020

Int. J. Med. Sci.

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Family with sequence similarity 83A (FAM83A) is a newly-found over-expressed oncogene in several types of cancers and associates with poor prognosis. However, the role that FAM83A may play in the carcinogenesis of non-small cell lung cancer (NSCLC) still needs to be defined. The present study aimed to investigate the function of FAM83A in NSCLC progression and to investigate the possible mechanism. Analysis of Gene Expression Omnibus (GEO) database and rt-PCR showed up-regulated expression of FAM83A in NSCLC. GEO and the Cancer Genome Atlas (TCGA) data analysis revealed that high expression level of FAM83A in NSCLC was associated with poor prognosis. In vitro experiments showed that depleting FAM83A by siRNA/shRNA significantly inhibited cell proliferation and induced cell apoptosis. Cell motility was also retarded after silencing FAM83A, as demonstrated by Transwell assay. FAM83A depletion in A549 cells also inhibited subcutaneous tumor growth and lung metastasis in vivo. Western blotting showed that silencing FAM83A decreased the phosphorylation of ERK and PI3K/Akt/mTOR. On the other hand, overexpressing FAM83A in vitro enhanced cell proliferation and invasiveness, which was repressed by PI3K inhibitor and ERK inhibitor separately. Taken together, our study suggests that FAM83A promotes tumorigenesis of NSCLC at least partly via ERK and PI3K/Akt/mTOR pathways, making it a promising therapeutic target.

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“…MYC, a proto-oncogene, was first discovered as the cellular homolog of the Avian virus myelocytomatosis oncogene and plays various roles in protein synthesis, metabolism, and cellular differentiation [25,26]. C-Myc, a transcription factor, is thought to regulate the expression of 15% of all genes by binding enhancer box sequences (E-boxes) [27]. Moreover, c-Myc can lead to genomic instability, gene amplification, cellular proliferation, and repression of apoptosis, which is observed in various tumors, including breast, lung, colon, and prostate cancers [25,27].…”

Section: Introductionmentioning

confidence: 99%

“…C-Myc, a transcription factor, is thought to regulate the expression of 15% of all genes by binding enhancer box sequences (E-boxes) [27]. Moreover, c-Myc can lead to genomic instability, gene amplification, cellular proliferation, and repression of apoptosis, which is observed in various tumors, including breast, lung, colon, and prostate cancers [25,27]. Although numerous studies have examined the interaction of PVT1 and MYC, the detailed mechanisms of the interaction between them remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA PVT1 interacts with MYC and its downstream molecules to synergistically promote tumorigenesis

Jin

Wang

Zhang

et al. 2019

Cell. Mol. Life Sci.

117

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Numerous studies have shown that non-coding RNAs play crucial roles in the development and progression of various tumor cells. Plasmacytoma variant translocation 1 (PVT1) mainly encodes a long non-coding RNA (lncRNA) and is located on chromosome 8q24.21, which constitutes a fragile site for genetic aberrations. PVT1 is well-known for its interaction with its neighbor MYC, which is a qualified oncogene that plays a vital role in tumorigenesis. In the past several decades, increasing attention has been paid to the interaction mechanism between PVT1 and MYC, which will benefit the clinical treatment and prognosis of patients. In this review, we summarize the coamplification of PVT1 and MYC in cancer, the positive feedback mechanism, and the latest promoter competition mechanism of PVT1 and MYC, as well as how PVT1 participates in the downstream signaling pathway of c-Myc by regulating key molecules. We also briefly describe the treatment prospects and research directions of PVT1 and MYC.

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Recent advances in searching c-Myc transcriptional cofactors during tumorigenesis

Cited by 44 publications

References 71 publications

Cisplatin-mediated down-regulation of miR-145 contributes to up-regulation of PD-L1 via the c-Myc transcription factor in cisplatin-resistant ovarian carcinoma cells

Cisplatin-mediated down-regulation of miR-145 contributes to up-regulation of PD-L1 via the c-Myc transcription factor in cisplatin-resistant ovarian carcinoma cells

FAM83A is amplified and promotes tumorigenicity in non-small cell lung cancer via ERK and PI3K/Akt/mTOR pathways

Long non-coding RNA PVT1 interacts with MYC and its downstream molecules to synergistically promote tumorigenesis

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