Abacavir induces the transcriptional activity of YY1 and other oncogenic transcription factors in gastric cancer cells

Panneerpandian, Ponmathi; Devanandan, Helen Jemimah; Marimuthu, Anantharaj; Karthikeyan, Chandrabose; Ganesan, Kumaresan

doi:10.1016/j.antiviral.2019.104695

Cited by 9 publications

(4 citation statements)

References 29 publications

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“…Wu et al (11) reported that microRNA (miR)-489 targets downregulation of lactate dehydrogenase A (LDHA)-mediated aerobic glycolysis to inhibit multiple myeloma cell invasion and proliferation. Transcription factor yin yang 1 (YY1) can bind to gene promoters in a variety of cells, regulating downstream transcription and thereby affecting protein expression (12). Numerous reports (13)(14)(15) have demonstrated that YY1 is significantly upregulated in a variety of types of cancer, including breast cancer, lung cancer and glioma.…”

Section: Introductionmentioning

confidence: 99%

YY1 transcription factor induces proliferation and aerobic glycolysis of neuroblastoma cells via LDHA regulation

et al. 2022

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The present study investigated the effect of transcription factor yin yang 1 (YY1) on aerobic glycolysis and cell proliferation in neuroblastoma and its mechanism. Neuroblastoma cell lines were used to investigate the association between YY1 and lactate dehydrogenase A (LDHA) expression. Cell Counting Kit (CCK)-8 and clone formation experiments were used to detect the cell viability. The interaction of YY1 and LDHA was detected using chromatin immunoprecipitation assay. Glucose uptake, intra/extracellular lactate and pyruvate and LDHA expression were evaluated using standard methods. Reverse transcription quantitative PCR, western blotting and gene overexpression or silencing were undertaken to explore the biological effects and underlying mechanisms of transcriptional regulators in NB cells. The results demonstrated that YY1 was significantly upregulated in neuroblastoma cell lines. The results of aerobic glycolysis and CCK-8 indicated that YY1 significantly promoted the proliferation and aerobic glycolysis of neuroblastoma cells. In addition, chromatin immunoprecipitation-PCR results demonstrated that YY1 was directly bound to the promoter LDHA. Overexpression of LDHA could reverse the inhibitory effect of sh-YY1 on aerobic glycolysis and proliferation of neuroblastoma cells. In conclusion, YY1 could induce aerobic glycolysis and proliferation of neuroblastoma cell lines, and may directly mediate the regulation of LDHA. These findings may provide novel insight for the treatment of neuroblastoma.

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Section: Introductionmentioning

confidence: 99%

YY1 transcription factor induces proliferation and aerobic glycolysis of neuroblastoma cells via LDHA regulation

et al. 2022

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“…Previous studies have demonstrated the close association between YY1 expression and the prognosis of various cancers [32] . Additionally, YY1 can promote the proliferation and metastasis of GC via multiple cancer-related pathways [33][34][35][36][37][38] . YY1 can also induce immune therapy resistance through p53, miR34a, STAT3, NF-kB, PI3K/AKT/mTOR, c-Myc, and COX-2 [39] .…”

Section: Discussionmentioning

confidence: 99%

YY1: a key regulator inhibits gastric cancer ferroptosis and mediating Apatinib-resistance

Geng

Chen

et al. 2023

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Background Gastric cancer (GC) is one of the most common and lethal cancers worldwide. Apatinib, a preoperative neoadjuvant therapy, has limited efficacy in GC patients with high YY1 expression. YY1 is associated with poor prognosis, drug resistance and metastasis in GC, but its mechanisms are unclear. Results We observed that higher YY1 expression levels were associated with lower postoperative progression-free survival (PFS) and disease-specific survival (DSS) rates based on the TCGA analysis. Moreover, YY1 expression was found to be an independent indicator of DSS in GC patients. Additionally, YY1 expression was significantly higher in tumor tissues compared to adjacent normal tissues. Bioinformatics analysis revealed significant differentially expressed genes (DEGs), transcriptional targets, transcription factors, and co-expressed genes related to YY1. Through LASSO Cox analysis, we identified Transferrin as a potential key protein regulated by YY1, and its high expression was correlated with adverse DSS and PFS outcomes. Further analysis showed that YY1 regulated the activity of the p53 signaling pathway and ferroptosis in GC cells. The study also revealed that YY1 overexpression suppressed immune cell infiltration in GC tumors. Furthermore, the study demonstrated that YY1 overexpression inhibited GC cell ferroptosis and mediated Apatinib resistance through the p53 signaling pathway. IFN-a reverses Apatinib resistance and immune suppression in GC tissues. Conclusions Our findings suggest that YY1 plays a crucial role in GC progression and prognosis and may serve as a potential therapeutic target for improving patient outcomes.

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“…TERT extends telomere length to an extent that correlates with the proliferation capacity of both normal and cancerous cells, and telomerase activation upon TERT production widely occurs in human malignant cells, which is essential for malignant transformation ( 29 ). The presence of co-activation of TERT and YY1 was determined in a subset of gastric tumors ( 30 ). Meanwhile, YY1 adversely modulates GAS5 expression by binding to the GAS5 promoter and thus represses its transcription in neurons following cerebral ischemia/reperfusion injury ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

YY1 Promotes Telomerase Activity and Laryngeal Squamous Cell Carcinoma Progression Through Impairment of GAS5-Mediated p53 Stability

et al. 2021

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Yin Yang 1 (YY1) is a key transcription factor that exerts functional roles in the cell biological process of various cancers. The current study aimed to elucidate the role and mechanism of YY1 in laryngeal squamous cell carcinoma (LSCC). YY1 mRNA and protein expression in human LSCC cell lines was detected by RT-qPCR and Western blot analysis. An interaction of YY1, GAS5, and p53 protein stability was predicted and confirmed by bioinformatics, ChIP, Co-IP, RIP, and FISH assays. Following loss- and gain-function assays, LSCC cell proliferation, colony formation, cell cycle, telomere length and telomerase activity were evaluated by CCK-8 assay, colony formation assay, flow cytometry, and PCR-ELISA, respectively. Nude mice were xenografted with the tumor in vivo. LSCC cell lines presented with upregulated expression of YY1, downregulated GAS5 expression, and decreased p53 stability. YY1 inhibited the expression of GAS5, which in turn recruited p300 and bound to p53, thus stabilizing it. Moreover, YY1 could directly interact with p300 and suppressp53 stability, leading to enhancement of cell proliferation, telomere length and telomerase activity in vitro along with tumor growth in vivo. Collectively, YY1 can stimulate proliferation and telomerase activity of LSCC cells through suppression of GAS5-dependent p53 stabilization or by decreasing p53 stability via a direct interaction with p300, suggesting that YY1 presents a therapeutic target as a potential oncogene in LSCC development and progression.

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Abacavir induces the transcriptional activity of YY1 and other oncogenic transcription factors in gastric cancer cells

Cited by 9 publications

References 29 publications

YY1 transcription factor induces proliferation and aerobic glycolysis of neuroblastoma cells via LDHA regulation

YY1 transcription factor induces proliferation and aerobic glycolysis of neuroblastoma cells via LDHA regulation

YY1: a key regulator inhibits gastric cancer ferroptosis and mediating Apatinib-resistance

YY1 Promotes Telomerase Activity and Laryngeal Squamous Cell Carcinoma Progression Through Impairment of GAS5-Mediated p53 Stability

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