PRMT6 promotes tumorigenicity and cisplatin response of lung cancer through triggering 6PGD/ENO1 mediated cell metabolism

Sun, Mingming; Li, Leilei; Niu, Yujia; Wang, Yingzhi; Yan, Qi; Xie, Fei; Qiao, Yaya; Song, Jiaqi; Sun, Huanran; Li, Zhen; Lai, Sizhen; Chang, Hongkai; Zhang, Han; Wang, Jiyan; Yang, Chenxin; Zhao, Huifang; Tan, Junzhen; Li, Yanping; Liu, Shuangping; Lü, Bin; Liu, Min; Kong, Guangyao; Zhao, Yiming; Zhang, Chunze; Lin, Shuhai; Luo, Cheng; Zhang, Shuai; Shan, Changliang

doi:10.1016/j.apsb.2022.05.019

Cited by 25 publications

(8 citation statements)

References 27 publications

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“…Interestingly, in our previous report, we demonstrated that PRMT6 asymmetrically dimethylates the R9 and R372 sites of ENO1 in lung cancer, 51 which is different from our finding in this study that PRMT5 only symmetrically dimethylates the R9 site of ENO1 in ovarian cancer. Although PRMT5 and PRMT6 are not the same type of PRMTs, there is a certain degree of similarity in the selection of substrate catalytic sites.…”

Section: Discussioncontrasting

confidence: 99%

“…Thus, the biological functions of PRMT5 binding to HK2 or GAPDH deserves further exploration, which would hopefully help us to broader implications for proving PRMT5 as a potential target for the treatment of ovarian cancer. Interestingly, in our previous report, we demonstrated that PRMT6 asymmetrically dimethylates the R9 and R372 sites of ENO1 in lung cancer, 51 which is different from our finding in this study that PRMT5 only symmetrically dimethylates the R9 site of ENO1 in ovarian cancer. Although PRMT5 and PRMT6 are not the same type of PRMTs, there is a certain degree of similarity in the selection of substrate catalytic sites.…”

Section: Discussioncontrasting

confidence: 99%

“…In addition, we found that the expression of PRMT5 was higher in lung cancer than in normal lung tissue. However, knockdown of PRMT5 promoted the proliferation of lung cancer cells 51 . In another report, 40 we found that the mRNA of PRMT6 in paclitaxel‐resistant ovarian cancer cells was lower than that in control ovarian cancer cells (Figure 6A and B).…”

Section: Discussionmentioning

confidence: 66%

“…However, knockdown of PRMT5 promoted the proliferation of lung cancer cells. 51 In another report, 40 we found that the mRNA of PRMT6 in paclitaxel‐resistant ovarian cancer cells was lower than that in control ovarian cancer cells (Figure 6A and B ). In this manuscript, PRMT5 is highly expressed in ovarian cancer cells, and the expression level is higher in paclitaxel‐resistant cells.…”

Section: Discussionmentioning

confidence: 72%

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PRMT5 promotes ovarian cancer growth through enhancing Warburg effect by methylating ENO1

Xie

Zhang

Zhu

et al. 2023

MedComm

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Protein arginine methyltransferase 5 (PRMT5) is a major type II enzyme responsible for symmetric dimethylation of arginine (SDMA), and plays predominantly roles in human cancers, including in ovarian cancer. However, the exactly roles and underlying mechanisms of PRMT5 contributing to the progression of ovarian cancer mediated by reprogramming cell metabolism remain largely elusive. Here, we report that PRMT5 is highly expressed and correlates with poor survival in ovarian cancer. Knockdown or pharmaceutical inhibition of PRMT5 is sufficient to decrease glycolysis flux, attenuate tumor growth, and enhance the antitumor effect of Taxol. Mechanistically, we find that PRMT5 symmetrically dimethylates alpha‐enolase (ENO1) at arginine 9 to promotes active ENO1 dimer formation, which increases glycolysis flux and accelerates tumor growth. Moreover, PRMT5 signals high glucose to increase the methylation modification of ENO1. Together, our data reveal a novel role of PRMT5 in promoting ovarian cancer growth by controlling glycolysis flux mediated by methylating ENO1, and highlights that PRMT5 may represent a promising therapeutic target for treating ovarian cancer.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 72%

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PRMT5 promotes ovarian cancer growth through enhancing Warburg effect by methylating ENO1

Xie

Zhang

Zhu

et al. 2023

MedComm

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“…Cell experiments confirmed that ZFP41 plays a crucial role in in cell viability, proliferation, migration and invasion. ZFP41 was also associated with aldoa, GadPH, PFKl, PKM and PGK1, which can promote glycolysis and malignancy (50)(51)(52)(53)(54)(55)(56). The present study also explored the association between ZFP41 and glycolysis in Hcc, and found that ZFP41 was a crucial factor in HCC glycolysis.…”

Section: Discussionmentioning

confidence: 60%

Combining a glycolysis‑related prognostic model based on scRNA‑Seq with experimental verification identifies ZFP41 as a potential prognostic biomarker for HCC

Teng,

Xu,

Wang

et al. 2024

Mol Med Rep

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Hepatocellular carcinoma (HCC) is a common malignancy with a poor prognosis, and its heterogeneity affects the response to clinical treatments. Glycolysis is highly associated with HCC therapy and prognosis. The present study aimed to identify a novel biomarker for HCC by exploring the heterogeneity of glycolysis in HCC. The intersection of both marker genes of glycolysis-related cell clusters from single-cell RNA sequencing analysis and mRNA data of liver HCC from The Cancer Genome Atlas were used to construct a prognostic model through Cox proportional hazard regression and the least absolute shrinkage and selection operator Cox regression. Data from the International Cancer Genome Consortium were used to validate the results of the analysis. Immune status analysis was then conducted. A significant gene in the prognostic model was identified as a potential biomarker and was verified through in vitro experiments. The results revealed that the glycolysis-related prognostic model divided patients with HCC into high- and low-risk groups. A nomogram combining the model and clinical features exhibited accurate predictive ability, with an area under the curve of 0.763 at 3 years. The high-risk group exhibited a higher expression of checkpoint genes and lower tumor immune dysfunction and exclusion scores, suggesting that this group may be more likely to benefit from immunotherapy. The tumor tissues had a higher zinc finger protein (ZFP)41 mRNA and protein expression compared with the adjacent tissues. In vitro analyses revealed that ZFP41 played a crucial role in cell viability, proliferation, migration, invasion and glycolysis. On the whole, the present study demonstrates that the glycolysis-related prognostic gene, ZFP41, is a potential prognostic biomarker and therapeutic target, and may play a crucial role in glycolysis and malignancy in HCC.

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Epigenetic regulation in cancer therapy: From mechanisms to clinical advances

Tao,

Zhou,

Luo

et al. 2024

MedComm – Oncology

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Epigenetic regulation refers to the alteration of gene expression independent of changes in DNA sequence. It involves chemical modifications such as DNA methylation, histone methylation, and histone acetylation, which are regulated by a coordinated interplay of various regulators to ensure precise spatial and temporal regulation of gene expression. Epigenetic aberrations are commonly observed in cancer and are considered as hallmarks of cancer. In recent years, small molecules targeting specific epigenetic regulators have been developed and are demonstrating promising therapeutic potential in preclinical and clinical trials for cancer treatment. In this review, we summarize the essential regulatory mechanisms and dysfunctions of epigenetic regulators involved in DNA methylation, histone methylation, and histone acetylation during tumor development and progression. Moreover, we discuss the current advances and challenges in cancer epigenetic therapy that target these mechanisms in both hematologic malignancies and solid tumors. Finally, we discuss the potential of combining epigenetic drugs with other therapies, including chemotherapy, radiotherapy, targeted therapy, and immunotherapy, as a promising approach for cancer treatment. Overall, we aim to enhance the understanding of epigenetic regulation in cancer therapy and explore targeted therapeutic strategies based on these mechanisms, to ultimately advance cancer therapy and improve patient prognosis.

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PRMT6 promotes tumorigenicity and cisplatin response of lung cancer through triggering 6PGD/ENO1 mediated cell metabolism

Cited by 25 publications

References 27 publications

PRMT5 promotes ovarian cancer growth through enhancing Warburg effect by methylating ENO1

PRMT5 promotes ovarian cancer growth through enhancing Warburg effect by methylating ENO1

Combining a glycolysis‑related prognostic model based on scRNA‑Seq with experimental verification identifies ZFP41 as a potential prognostic biomarker for HCC

Epigenetic regulation in cancer therapy: From mechanisms to clinical advances

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