LINC01232 Promotes Gastric Cancer Proliferation through Interacting with EZH2 to Inhibit the Transcription of KLF2

Liu, Jing; Li, Zhen; Yu, Guohua; Wang, Ting; Qu, Guimei; Wang, Yunhui

doi:10.4014/jmb.2106.06041

Cited by 10 publications

(6 citation statements)

References 23 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results found that not only in data from TCGA but also in our selected samples, LINC01232 was upregulated in gastric cancer tissues compared to para-cancer tissues. These results were in accordance with reported studied by Liu et al 18 …”

Section: Discussionsupporting

confidence: 94%

See 1 more Smart Citation

LINC01232 Promotes Metastasis and EMT by Regulating miR-506-5p/PAK1 Axis in Gastric Cancer

Chen¹,

Liao²,

Xu³

et al. 2022

CMAR

View full text Add to dashboard Cite

Background Long non-coding RNA LINC01232 plays an important role in the progression of metastasis in several cancers. However, the function of LINC01232 in gastric cancer is limited. Authors aimed to investigate the role and mechanism of LINC01232 in the metastasis of gastric cancer. Methods The expression levels and correlation of LINC01232, miR-506-5p, and PAK1 were analyzed by GEPIA or ENCORI, and the abundance of LINC01232 and miR-506-5p was measured in tissues and cells via qRT-PCR, the location of LINC01232 in gastric cells was analyzed by nuclear and cytoplasmic fractionation, while the protein levels of PAK1, E-cadherin and vimentin were additionally quantified by Western blotting. Interactions between LINC01232, miR-506-5p, and PAK1 were detected through luciferase reporter assays, qRT-PCR and Western blotting. Cellular viability was evaluated through CCK8 assays, migration ability was measured by transwell assays, invasion ability was tested by wound healing experiment. Results LINC01232 was overexpressed in gastric cancer tissues and cells, and mainly located in nucleus. The inhibition of LINC01232 could suppress migration, invasion and EMT of gastric cancer cells. MiR-506-5p was downregulated in gastric cancer tissues and cells. LINC01232 sponged miR-506-5p to accelerate migration and EMT. PAK1 was certified to be a target of miR-506-5p, inhibition of PAK1 could interrupt LINC01232 overexpression-induced migration of gastric cancer cells. Conclusion The LINC01232/miR-506-5p/PAK1 axis promotes metastasis of gastric cancer cells.

show abstract

Section: Discussionsupporting

confidence: 94%

“… 17 Recent study identified that LINC01232 promoted cell proliferation by interacting with EZH2 in gastric cancer. 18 However, the function of LINC01232 on metastasis and the possible mechanism is still unclear.…”

Section: Introductionmentioning

confidence: 99%

LINC01232 Promotes Metastasis and EMT by Regulating miR-506-5p/PAK1 Axis in Gastric Cancer

Chen¹,

Liao²,

Xu³

et al. 2022

CMAR

View full text Add to dashboard Cite

show abstract

“…The knockdown of LINC01232 is shown to suppress the proliferation of gastric-cancer cells both in vivo and in vitro. This finding suggests LINC01232’s potential as an effective therapeutic target for gastric cancer ( Table 2 ) [ 111 ].…”

Section: Discussionmentioning

confidence: 99%

Gastric Cancer in the Era of Epigenetics

Christodoulidis,

Koumarelas,

Kouliou

et al. 2024

IJMS

View full text Add to dashboard Cite

Gastric cancer (GC) remains a significant contributor to cancer-related mortality. Novel high-throughput techniques have enlightened the epigenetic mechanisms governing gene-expression regulation. Epigenetic characteristics contribute to molecular taxonomy and give rise to cancer-specific epigenetic patterns. Helicobacter pylori (Hp) infection has an impact on aberrant DNA methylation either through its pathogenic CagA protein or by inducing chronic inflammation. The hypomethylation of specific repetitive elements generates an epigenetic field effect early in tumorigenesis. Epstein–Barr virus (EBV) infection triggers DNA methylation by dysregulating DNA methyltransferases (DNMT) enzyme activity, while persistent Hp-EBV co-infection leads to aggressive tumor behavior. Distinct histone modifications are also responsible for oncogene upregulation and tumor-suppressor gene silencing in gastric carcinomas. While histone methylation and acetylation processes have been extensively studied, other less prevalent alterations contribute to the development and migration of gastric cancer via a complex network of interactions. Enzymes, such as Nicotinamide N-methyltransferase (NNMT), which is involved in tumor’s metabolic reprogramming, interact with methyltransferases and modify gene expression. Non-coding RNA molecules, including long non-coding RNAs, circular RNAs, and miRNAs serve as epigenetic regulators contributing to GC development, metastasis, poor outcomes and therapy resistance. Serum RNA molecules hold the potential to serve as non-invasive biomarkers for diagnostic, prognostic or therapeutic applications. Gastric fluids represent a valuable source to identify potential biomarkers with diagnostic use in terms of liquid biopsy. Ongoing clinical trials are currently evaluating the efficacy of next-generation epigenetic drugs, displaying promising outcomes. Various approaches including multiple miRNA inhibitors or targeted nanoparticles carrying epigenetic drugs are being designed to enhance existing treatment efficacy and overcome treatment resistance.

show abstract

“…PLZF then recruits EZH2 to increase H3K27 trimethylation at the PDGFB promoter, suppressing its expression and subsequently downregulating PI3K/Akt signaling 157 . Two additional lncRNAs, LINC01232 and LINC00202 , were found to be upregulated in GC, and they interacted with EZH2, negatively regulating the expression of KLF2 , a zinc-finger transcription factor, through histone methylation 158 , 159 . Another oncogenic lncRNA, HOTAIR , promoted EMT by recruiting PRC2 to catalyze H3K27me3 at the CDH1 promoter in GC 160 .…”

Section: Interaction Between Ncrnas and Histone Modification In Gastr...mentioning

confidence: 99%

Chromatin and noncoding RNA-mediated mechanisms of gastric tumorigenesis

2023

View full text Add to dashboard Cite

Gastric cancer (GC) is one of the most common and deadly cancers in the world. It is a multifactorial disease highly influenced by environmental factors, which include radiation, smoking, diet, and infectious pathogens. Accumulating evidence suggests that epigenetic regulators are frequently altered in GC, playing critical roles in gastric tumorigenesis. Epigenetic regulation involves DNA methylation, histone modification, and noncoding RNAs. While it is known that environmental factors cause widespread alterations in DNA methylation, promoting carcinogenesis, the chromatin- and noncoding RNA-mediated mechanisms of gastric tumorigenesis are still poorly understood. In this review, we focus on discussing recent discoveries addressing the roles of histone modifiers and noncoding RNAs and the mechanisms of their interactions in gastric tumorigenesis. A better understanding of epigenetic regulation would likely facilitate the development of novel therapeutic approaches targeting specific epigenetic regulators in GC.

show abstract

LINC01232 Promotes Gastric Cancer Proliferation through Interacting with EZH2 to Inhibit the Transcription of KLF2

Cited by 10 publications

References 23 publications

LINC01232 Promotes Metastasis and EMT by Regulating miR-506-5p/PAK1 Axis in Gastric Cancer

LINC01232 Promotes Metastasis and EMT by Regulating miR-506-5p/PAK1 Axis in Gastric Cancer

Gastric Cancer in the Era of Epigenetics

Chromatin and noncoding RNA-mediated mechanisms of gastric tumorigenesis

Contact Info

Product

Resources

About