LINC00114 stimulates growth and glycolysis of esophageal cancer cells by recruiting EZH2 to enhance H3K27me3 of DLC1

Qin, Jianzhang; Li, Yishuai; Li, Zhe; Qin, Xuebo; Zhou, Xuetao; Zhang, Hao; Li, Shujun

doi:10.1186/s13148-022-01258-y

Cited by 8 publications

(5 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Significantly downregulated genes in Tks4 KO cells include EHF, RERG, MMP13, MMP14, BMP5, and DLC1 ( Figure 2 C). These genes are involved in epithelial differentiation and proliferation [ 40 ] and tumor development, with low expression connected to poor prognosis [ 41 , 42 , 43 ].…”

Section: Resultsmentioning

confidence: 99%

Absence of Scaffold Protein Tks4 Disrupts Several Signaling Pathways in Colon Cancer Cells

Jacksi

Schád

Buday

et al. 2023

IJMS

View full text Add to dashboard Cite

Tks4 is a large scaffold protein in the EGFR signal transduction pathway that is involved in several cellular processes, such as cellular motility, reactive oxygen species-dependent processes, and embryonic development. It is also implicated in a rare developmental disorder, Frank–ter Haar syndrome. Loss of Tks4 resulted in the induction of an EMT-like process, with increased motility and overexpression of EMT markers in colorectal carcinoma cells. In this work, we explored the broader effects of deletion of Tks4 on the gene expression pattern of HCT116 colorectal carcinoma cells by transcriptome sequencing of wild-type and Tks4 knockout (KO) cells. We identified several protein coding genes with altered mRNA levels in the Tks4 KO cell line, as well as a set of long non-coding RNAs, and confirmed these changes with quantitative PCR on a selected set of genes. Our results show a significant perturbation of gene expression upon the deletion of Tks4, suggesting the involvement of different signal transduction pathways over the well-known EGFR signaling.

show abstract

Section: Resultsmentioning

confidence: 99%

Absence of Scaffold Protein Tks4 Disrupts Several Signaling Pathways in Colon Cancer Cells

Jacksi

Schád

Buday

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“…We also found that LINC00114 was significantly upregulated in B-ALL compared to T-ALL ( Table 3 ). Additionally, LINC00114 has been shown to play a role in the development of colorectal cancer [88] and esophageal cancer [89]. ENSG00000227706 has been demonstrated to be associated with multiple myeloma [90] and acute myeloid leukemia [91] and overexpressed in leukemia [92,93].…”

Section: Resultsmentioning

confidence: 99%

Data-driven discovery of gene expression markers distinguishing pediatric acute lymphoblastic leukemia subtypes

Nourbakhsh,

Tom,

Schrøder Lassen

et al. 2024

Preprint

View full text Add to dashboard Cite

Acute lymphoblastic leukemia (ALL), the most common cancer in children, is overall divided into two subtypes, B-cell precursor ALL (B-ALL) and T-cell ALL (T-ALL), which have different molecular characteristics. Despite massive progress in understanding the disease trajectories of ALL, ALL remains a major cause of death in children. Thus, further research exploring the biological foundations of ALL is essential. Here, we examined the diagnostic, prognostic, and therapeutic potential of gene expression data in pediatric patients with ALL. We discovered a subset of expression markers differentiating B- and T-ALL:CCN2,VPREB3,NDST3,EBF1, RN7SKP185, RN7SKP291, SNORA73B, RN7SKP255, SNORA74A, RN7SKP48, RN7SKP80, LINC00114, a novel gene (ENSG00000227706), and 7SK. The expression level of these markers all demonstrated significant effects on survival of the patients, comparing the two subtypes. We also discovered four expression subgroups in the expression data with eight genes driving separation between two of these predicted subgroups. A subset of the 14 markers could separate B- and T-ALL in an independent cohort of patients with ALL. This study can enhance our knowledge of the transcriptomic profile of different ALL subtypes.

show abstract

“…We demonstrated that PRMT1 could deposit ADMA at SHMT2-R315, and this methylation enhanced SHMT2 protein activity. (4) Excessive accumulation of methylation signals of SHMT2 promoted the levels of glycolysis and indicators related to one-carbon metabolism in ESCA cells. In conclusion, our data revealed an alternative mechanism by which PRMT1 mediated aerobic glycolysis in ESCA, which drove esophageal carcinogenesis by methylating SHMT2.…”

Section: Discussionmentioning

confidence: 99%

“…The frequently reported short survival is mainly attributed to the limited bene t of systemic radiotherapy and the increased incidence of margin involvement in surgical specimens [3]. Notably, surgery combined with chemotherapy remains the preferred treatment for this speci c population of patients with advanced ESCA, but more efforts should be devoted to elucidating the speci c mechanisms of disease progression and establishing mechanism-based therapeutic strategies for patients with potential clinical consequences (recurrence or metastasis) [4,5]. Therefore, the study of tumor biomarkers is a promising approach to control disease progression.…”

Section: Introductionmentioning

confidence: 99%

SHMT2 arginine methylation by PRMT1 facilitates esophageal cancer progression by enhancing glycolysis and one-carbon metabolism

Qiao,

Li,

Cheng

et al. 2023

Preprint

View full text Add to dashboard Cite

Background Protein arginine methyltransferase 1 (PRMT1) is the main enzyme that directly responsible for the production of asymmetric dimethylarginine (ADMA), and upregulation of PRMT1 is observed in a variety of malignancies, including esophageal cancer (ESCA). Dysregulation of arginine methylation caused by PRMT1 overexpression is a driver of poor cancer progression, and the detailed mechanism of modulation is currently unknown. Results The present study confirmed a novel oncogenic mechanism of PRMT1 in ESCA. PRMT1 levels were significantly upregulated in ESCA, and its high expression correlated with TNM stage and poor patient prognosis. We continued to find the mechanisms by which PRMT1 expression was more relevant to ESCA progression. RNA-seq and KEGG enrichment analyses revealed that differentially expressed genes after PRMT1 silencing in ESCA might modulate serine/one-carbon metabolism. Knockdown of PRMT1 in vitro resulted in a significant reduction in ESCA cell growth, and indicators related to serine/one-carbon metabolism and glycolysis, whereas its overexpression showed opposite results. The catalytic activity of PRMT1 was crucial in mediating these biological processes. We found that PRMT1 mediated the ADMA modification of serine hydroxymethyltransferase 2 (SHMT2) at arginine 415 (R415), which activated SHMT2 activity and enhanced serine/one-carbon metabolism and glycolysis. The R415K mutation largely eliminated the arginine methylation of SHMT2 by PRMT1, and weakened PRMT1-induced glycolysis and serine/one-carbon metabolism. Conclusion Our study further confirmed the link between the two proteins, PRMT1 and SHMT2, as well as arginine methylation and glycolysis. The study of deeper molecular mechanisms will reveal a broader role of arginine methylation in the regulation of glycolysis.

show abstract

LINC00114 stimulates growth and glycolysis of esophageal cancer cells by recruiting EZH2 to enhance H3K27me3 of DLC1

Cited by 8 publications

References 58 publications

Absence of Scaffold Protein Tks4 Disrupts Several Signaling Pathways in Colon Cancer Cells

Absence of Scaffold Protein Tks4 Disrupts Several Signaling Pathways in Colon Cancer Cells

Data-driven discovery of gene expression markers distinguishing pediatric acute lymphoblastic leukemia subtypes

SHMT2 arginine methylation by PRMT1 facilitates esophageal cancer progression by enhancing glycolysis and one-carbon metabolism

Contact Info

Product

Resources

About