The lncRNA LINC01605 promotes the progression of pancreatic ductal adenocarcinoma by activating the mTOR signaling pathway DOI Creative Commons

Yu-Heng Zhu,

Qin-Yuan Jia,

Hong-Fei Yao

et al.

Research Square (Research Square), Journal Year: 2023, Volume and Issue: unknown

Published: Nov. 8, 2023

Abstract Background This study investigated the molecular mechanism of long intergenic non-protein coding RNA 1605 (LINC01605) in process tumor growth and liver metastasis pancreatic ductal adenocarcinoma (PDAC). Methods LINC01605 was filtered out with specificity through TCGA datasets (related to DFS) our RNA-sequencing data PDAC tissue samples from Renji Hospital. The expression level clinical relevance were then verified cohorts by immunohistochemical staining assay survival analysis. Loss- gain-of-function experiments performed estimate regulatory effects in vitro. RNA-seq LINC01605-knockdown cells subsequent inhibitor-based cellular function, western blotting, immunofluorescence rescue conducted explore mechanisms which regulates behaviors cells. Subcutaneous xenograft models intrasplenic employed its role vivo. Results is upregulated both primary tissues correlates poor prognosis. Loss gain function demonstrated that promotes proliferation migration In verification experiments, we found contributes progression cholesterol metabolism regulation a LIN28B-interacting manner activating mTOR signaling pathway. Furthermore, animal showed facilitates metastatic invasion Conclusions Our results indicate lncRNA cell regulating via activation pathway manner. These findings provide new insight into as well value for approaches metabolic therapeutic target PDAC.

Language: Английский

LINC01605 Is a Novel Target of Mutant p53 in Breast and Ovarian Cancer Cell Lines DOI Open Access
Michela Coan, Martina Toso, Laura Cesaratto

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(18), P. 13736 - 13736

Published: Sept. 6, 2023

TP53 is the most frequently mutated gene in human cancers. Most genomic alterations are missense mutations, which cause a loss of its tumour suppressor functions while providing mutant p53 (mut_p53) with oncogenic features (gain-of-function). Loss alters transcription both protein-coding and non-protein-coding genes. Gain-of-function mut_p53 triggers modification expression as well; however, impact on genes whether these affect properties cancer cell lines not fully explored. In this study, we suggested that LINC01605 (also known lincDUSP) long non-coding RNA regulated by proved directly regulates binding to an enhancer region downstream locus. We also showed or downregulation impairs migration breast line. Eventually, performing combined analysis RNA-seq data generated mut_TP53-silenced knockout cells, share common pathways. Overall, our findings underline importance ncRNAs network ovarian particular pro-migratory

Language: Английский

Citations

2
The emerging role of m6A modification of non-coding RNA in gastrointestinal cancers: a comprehensive review DOI Creative Commons
Meiqi Wang, Zhuo Liu, Xuedong Fang

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2023, Volume and Issue: 11

Published: Oct. 30, 2023

Gastrointestinal (GI) cancer is a series of malignant tumors with high incidence globally. Although approaches for tumor diagnosis and therapy have advanced substantially, the mechanisms underlying occurrence progression GI are still unclear. Increasing evidence supports an important role N 6 -methyladenosine (m A) modification in many biological processes, including cancer-related processes via splicing, export, degradation, translation mRNAs. Under distinct contexts, m A regulators different expression patterns can regulate or be regulated by mRNAs non-coding RNAs, especially long RNAs. The roles development attracted increasing attention epigenetics research. In this review, we synthesize progress our understanding its cancer, esophageal, gastric, colorectal cancers. Furthermore, clarify mechanism which contributes to providing basis diagnostic, prognostic, therapeutic targets.

Language: Английский

Citations

1
LINC01605 promotes malignant phenotypes of cervical cancer via miR-149-3p/WNT7B axis DOI
Xiaoyu Kong,

Yuanpeng Xiong,

Liping Li

et al.

Gene, Journal Year: 2024, Volume and Issue: 921, P. 148518 - 148518

Published: May 10, 2024

Language: Английский

Citations

0
The lncRNA LINC01605 promotes the progression of pancreatic ductal adenocarcinoma by activating the mTOR signaling pathway DOI Creative Commons

Yu-Heng Zhu,

Qin-Yuan Jia,

Hong-Fei Yao

et al.

Cancer Cell International, Journal Year: 2024, Volume and Issue: 24(1)

Published: July 24, 2024

Abstract Background This study investigated the molecular mechanism of long intergenic non-protein coding RNA 1605 (LINC01605) in process tumor growth and liver metastasis pancreatic ductal adenocarcinoma (PDAC). Methods LINC01605 was filtered out with specificity through TCGA datasets (related to DFS) our RNA-sequencing data PDAC tissue samples from Renji Hospital. The expression level clinical relevance were then verified cohorts by immunohistochemical staining assay survival analysis. Loss- gain-of-function experiments performed estimate regulatory effects vitro. RNA-seq LINC01605-knockdown cells subsequent inhibitor-based cellular function, western blotting, immunofluorescence rescue conducted explore mechanisms which regulates behaviors cells. Subcutaneous xenograft models intrasplenic employed its role vivo. Results is upregulated both primary tissues correlates poor prognosis. Loss gain function demonstrated that promotes proliferation migration In verification experiments, we found contributes progression cholesterol metabolism regulation a LIN28B-interacting manner activating mTOR signaling pathway. Furthermore, animal showed facilitates metastatic invasion Conclusions Our results indicate lncRNA cell regulating via activation pathway manner. These findings provide new insight into as well value for approaches metabolic therapeutic target PDAC.

Language: Английский

Citations

0
Decreased expression of thyroid hormone receptor beta (THRB) indicates a poor prognostic factor for liver cancer DOI Creative Commons
Hao Zhou, Weijie Wang,

Ruopeng Liang

et al.

Research Square (Research Square), Journal Year: 2023, Volume and Issue: unknown

Published: July 11, 2023

Abstract Background: The reduced expression of Thyroid hormone receptors (TRs) which are encoded by two genes, THRA and THRB, is found in many human malignancies; however, the clinical prognostic value TRs patients with hepatocellular carcinoma (HCC) remains unclear. Methods: Kaplan-Meier analysis based on TCGA profile was performed. HCC tumors evaluated GEO databases R software. correlation between THRB immune cell infiltration analyzed TIMER 2.0 database. Results: demonstrated that low significantly associated worsened overall survival (OS) disease-specific ( P < 0.05), not THRA. Subgroup showed 1-year, 3-year, 5-year OS (all 0.05). In addition, values downregulation for were more significant hepatitis-virus = 0.0012), Asian race 0.0038) male 0.002), both with- without-alcohol-consumption 0.0234 0.0199, respectively). We down-regulated compared nontumor tissues 3 series (GSE14520, GSE77314, GSE84005) profile, but other 2 (GSE45436, GSE60502) had no down-regulation tumors. further calculated proportion paired samples 4 56.93% THRB. Immune resulted neutrophils top tumor infiltrating type Conclusions: rather than correlated worse patients.

Language: Английский

Citations

0
The lncRNA LINC01605 promotes the progression of pancreatic ductal adenocarcinoma by activating the mTOR signaling pathway DOI Creative Commons

Yu-Heng Zhu,

Qin-Yuan Jia,

Hong-Fei Yao

et al.

Research Square (Research Square), Journal Year: 2023, Volume and Issue: unknown

Published: Nov. 8, 2023

Abstract Background This study investigated the molecular mechanism of long intergenic non-protein coding RNA 1605 (LINC01605) in process tumor growth and liver metastasis pancreatic ductal adenocarcinoma (PDAC). Methods LINC01605 was filtered out with specificity through TCGA datasets (related to DFS) our RNA-sequencing data PDAC tissue samples from Renji Hospital. The expression level clinical relevance were then verified cohorts by immunohistochemical staining assay survival analysis. Loss- gain-of-function experiments performed estimate regulatory effects in vitro. RNA-seq LINC01605-knockdown cells subsequent inhibitor-based cellular function, western blotting, immunofluorescence rescue conducted explore mechanisms which regulates behaviors cells. Subcutaneous xenograft models intrasplenic employed its role vivo. Results is upregulated both primary tissues correlates poor prognosis. Loss gain function demonstrated that promotes proliferation migration In verification experiments, we found contributes progression cholesterol metabolism regulation a LIN28B-interacting manner activating mTOR signaling pathway. Furthermore, animal showed facilitates metastatic invasion Conclusions Our results indicate lncRNA cell regulating via activation pathway manner. These findings provide new insight into as well value for approaches metabolic therapeutic target PDAC.

Language: Английский

Citations

0