HNRNPC stabilizes m6A-modified AC145207.5 to accelerate tumorigenesis in colorectal cancer by impeding the Nrf2/GPX4 axis-mediated ferroptosis DOI Creative Commons
Dan Liu, Shanshan Lin,

Yueben Hu

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 23, 2024

Abstract Ferroptosis, an apoptosis-independent cell death pathway characterized by heightened lipid peroxidation, which holds promise for tumor suppression. Despite extensive research on long non-coding RNAs (LncRNAs) in ferroptosis, their role colorectal cancer (CRC) remains underexplored. We investigated the upregulation of AC145207.5 and HNRNPC expression CRC tissues through public dataset analysis in-house validation, identifying them as having significant diagnostic potential. In vitro experiments including MTS assay, transwell, colony formation, alongside in vivo studies using xenograft models, elucidated synergistic carcinogenic HNRNPC/AC145207.5 axis promoting malignant characteristics CRC. Mechanistically, m6A reader stabilized m6A-modified AC145207.5, contributing to its stabilization upregulation. Consequently, activated Nrf2/GPX4 axis, resulting increased GPX4 expression, inhibition GPX4-mediated facilitation progression. Our findings underscore clinical relevance illuminate regulatory suggesting implications targeted precision medicine

Language: Английский

STAT3-related lncRNAs in colorectal cancer progression; special focus on immune cell’s evasion DOI

Mohamed J. Saadh,

Junainah Abd Hamid,

H. Malathi

et al.

Pathology - Research and Practice, Journal Year: 2025, Volume and Issue: 266, P. 155810 - 155810

Published: Jan. 5, 2025

Language: Английский

Citations

0
N6-Methylandenosine-related lncRNAs as potential biomarkers for predicting prognosis and the immunotherapy response in pancreatic cancer DOI Creative Commons
Zhihui Bai,

Qianlin Xia,

Wanli Xu

et al.

Cellular and Molecular Life Sciences, Journal Year: 2025, Volume and Issue: 82(1)

Published: Jan. 21, 2025

Emerging evidence has shown that the N6-methyladenosine (m6A) modification of RNA plays key roles in tumorigenesis and progression various cancers. However, potential m6A long noncoding RNAs (lncRNAs) pancreatic cancer (PaCa) are still unknown. To analyze prognostic value m6A-related lncRNAs PaCa, an lncRNA signature was constructed as a risk model via Pearson's correlation univariate Cox regression analyses The Cancer Genome Atlas (TCGA) database. tumor microenvironment (TME), mutation burden, drug sensitivity PaCa were investigated by score analyses. We established consisting five lncRNAs, namely, LINC01091, AC096733.2, AC092171.5, AC015660.1, AC005332.6, which not only revealed significant differences immune cell infiltration associated with TME between high-risk low-risk groups but also predicted benefit immunotherapy for patients PaCa. Drugs such WZ8040, selumetinib, bortezomib identified more effective patients. Our results indicate could be independent indicator, may provide valuable insights identifying therapeutic approaches

Language: Английский

Citations

0
LINC00942 Accelerates Esophageal Cancer Progression by Raising PRKDC Through Interaction With PTBP1 DOI
Zhongqiu Wang, Shuo Li,

Xing Zhang

et al.

Journal of Biochemical and Molecular Toxicology, Journal Year: 2025, Volume and Issue: 39(3)

Published: March 1, 2025

ABSTRACT Aberrantly expressed LINC00942 is participated in the progression of several cancers. However, function esophageal cancer (ESCA) unclear. The objective this study was to explore effect on ESCA and its possible molecular mechanisms. First, differentially lncRNAs were analyzed using GSE192662 microarray. catRAPID omics v2.1 applied predict proteins that might interact with LINC00942. SDS‐PAGE silver staining assay, RNA pull down, RIP assay utilized validate interacting Then, seq detect downstream targets PTBP1, KEGG enrichment analysis used analyze genes involved proliferation migration‐related signaling pathways. In addition, CCK‐8, EdU transwell impact cell function. Bioinformatics revealed significantly overexpressed ESCA. Patients low‐expression had an obviously better prognosis. After knockdown, migration TE‐1 OE19 dramatically reduced. Subsequently, PTBP1 found LINC00942, PRKDC a target PTBP1. Functional showed markedly elevated after overexpression, knockdown reversed effect. Mechanistically, promoted expression by summary, facilitated cells via binding promote expression.

Language: Английский

Citations

0
GART promotes the proliferation and migration of human non-small cell lung cancer cell lines A549 and H1299 by targeting PAICS-Akt-β-catenin pathway DOI Creative Commons
Zhuo Chen,

Yu-Heng Ding,

Manyu Zhao

et al.

Frontiers in Oncology, Journal Year: 2025, Volume and Issue: 15

Published: March 25, 2025

Background Lung adenocarcinoma (LUAD) is the primary subtype of Non-small cell lung cancer (NSCLC) and a serious threat to human health. However, precise molecular mechanisms in remain largely unexplored. Methods Herein, we performed proteomic analysis cohort 20 LC tumors their paired normal tissues. The expression levels prognostic value hub proteins were also explored LUAD using public databases. Glycinamide ribonucleotide transformylase (GART) was detected by qRT-PCR lines. roles GART assessed CCK-8, colony formation, Wound healing assays, xenograft tumor model. Expression PAICS-Akt-β-catenin pathway estimated through western blot assays. Results tissues indicated that 263 upregulated 194 downregulated. Bioinformatics showed differentially expressed mainly associated with regulation apoptotic process adhesion, PI3K-Akt signaling pathway, Purine metabolism, Wnt pathway. EPRS, GART, HSPE1, RPS6 much higher than analyzed Ualcan database. Overexpression represented poor prognosis patients. Additionally, knockdown effectively inhibited proliferation migration cells both vitro vivo. Mechanistically, analyses suggested deletion could inhibit activation vivo . Conclusions Our study tumor-promoting function axis, it may be used as therapeutic target for NSCLC.

Language: Английский

Citations

0
An HRL‐SC/HIF‐1α positive feedback loop enhances cell proliferation, migration and angiogenesis in dental pulp stem cells via PI3K/AKT signalling pathway DOI Open Access
Junkai Zeng, Yeqing Yang, Chong Jiang

et al.

International Endodontic Journal, Journal Year: 2025, Volume and Issue: unknown

Published: March 28, 2025

Abstract Aim Dental pulp stem cells (DPSCs) are essential for regeneration but face low survival rates after transplantation. Genetic modification before transplantation is a promising solution to this issue. We aim elucidate the biological function and regulatory mechanism of hypoxic lncRNA HRL‐SC in DPSCs. Methodology The functions hypoxia inducible factor‐1α (HIF‐1α) DPSCs were evaluated vitro by cell proliferation, migration tube formation assays. Subcutaneous nude mice was used evaluate effect on DPSC viability vivo. RNA sequencing bioinformatics analysis, immunoprecipitation, dual luciferase reporter gene assay, co‐immunoprecipitation, fluorescence situ hybridization, immunofluorescence protein stability assays explore potential Data analysed one‐way analysis variance ( anova ) or Student's t ‐test, with p <.05 indicating statistical significance. Results HRL‐SC, hypoxia‐responsive lncRNA, enhanced abilities dental blocks revealed that HRL‐SC‐mediated exhibited improved elevated expression Ki‐67 CD31, along capacity form vascular‐like structures. HIF‐1α observed induce transcription HRL‐SC. Reciprocally, bound VHL, thereby inhibiting VHL‐mediated ubiquitination, which resulted positive feed‐forward loop HRL‐SC/HIF‐1α. RNA‐sequencing functional analyses closely associated hypoxia, angiogenesis, regeneration, integrin PI3K/AKT signalling pathways. Furthermore, shown stabilize ITGAV ITGB3 through PTBP1. Finally, it confirmed activated pathway via αvβ3/FAK HIF‐1α/PDK1 axes. Conclusions modified demonstrated signaling characteristics endothelial cells, may provide novel strategy application regeneration.

Language: Английский

Citations

0
HNRNPC stabilizes m6A-modified AC145207.5 to accelerate tumorigenesis in colorectal cancer by impeding the Nrf2/GPX4 axis-mediated ferroptosis DOI Creative Commons
Dan Liu, Shanshan Lin,

Yueben Hu

et al.

Non-coding RNA Research, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

0
Latest Update on lncRNA in Epithelial Ovarian Cancer—A Scoping Review DOI Creative Commons
Katarzyna Kwas, Maria Szubert, Jacek R. Wilczyński

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(7), P. 555 - 555

Published: April 7, 2025

Long noncoding RNAs (lncRNAs) are RNA molecules exceeding 200 nucleotides that do not encode proteins yet play critical roles in regulating gene expression at multiple levels, such as chromatin modification and transcription. These significantly engaged cancer progression, development, metastasis, chemoresistance. However, the function of lncRNAs epithelial ovarian (EOC) has been thoroughly studied. EOC remains challenging due to its complex molecular pathogenesis, characterized by genetic epigenetic alterations. Emerging evidence suggests lncRNAs, XIST, H19, NEAT1, MALAT1, involved modulating signaling pathways, influencing processes like cell proliferation, invasion, migration, Despite extensive research, precise mechanism acting pathogenesis treatment resistance still needs be fully understood, highlighting need for further studies. This review aims provide an updated overview current understanding EOC, emphasizing their potential biomarkers therapeutic targets. We point out gaps knowledge regarding lncRNAs’ influence on (EOC), deliberating new possible research areas.

Language: Английский

Citations

0
LINC00323 knockdown suppresses the proliferation, migration, and vascular mimicry of non-small cell lung cancer cells by promoting ubiquitinated degradation of AKAP1 DOI Creative Commons
Bin Ke, Hai Zhong,

Yuxin Gong

et al.

Non-coding RNA Research, Journal Year: 2024, Volume and Issue: 11, P. 131 - 140

Published: Dec. 14, 2024

LINC00323, a new long noncoding RNA, is aberrantly expressed in several cancers. However, the expression, function, and mechanism of LINC00323 non-small cell lung cancer (NSCLC) are unclear. In present study, VEGFA, microvessel density (MVD), AKAP1 levels were confirmed NSCLC tissues. Cell proliferation, migration, vascular mimicry (VM) examined to assess effects on cells. addition, interaction between was verified by RNA pull-down, LC-MS/MS immunoprecipitation. The ubiquitination level also through coimmunoprecipitation, cycloheximide (CHX) chase, assays vitro. Our results revealed that upregulated tissues positively correlated with metastasis, poor prognosis, VEGFA elevated MVD, expression. Functionally, or knockdown suppressed VM Mechanistically, could target AKAP1, accelerated ubiquitination-mediated protein degradation. Moreover, silencing progression downregulating AKAP1. prevents formation targeting indicating might be biological targets for treatment.

Language: Английский

Citations

0
HNRNPC stabilizes m6A-modified AC145207.5 to accelerate tumorigenesis in colorectal cancer by impeding the Nrf2/GPX4 axis-mediated ferroptosis DOI Creative Commons
Dan Liu, Shanshan Lin,

Yueben Hu

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 23, 2024

Abstract Ferroptosis, an apoptosis-independent cell death pathway characterized by heightened lipid peroxidation, which holds promise for tumor suppression. Despite extensive research on long non-coding RNAs (LncRNAs) in ferroptosis, their role colorectal cancer (CRC) remains underexplored. We investigated the upregulation of AC145207.5 and HNRNPC expression CRC tissues through public dataset analysis in-house validation, identifying them as having significant diagnostic potential. In vitro experiments including MTS assay, transwell, colony formation, alongside in vivo studies using xenograft models, elucidated synergistic carcinogenic HNRNPC/AC145207.5 axis promoting malignant characteristics CRC. Mechanistically, m6A reader stabilized m6A-modified AC145207.5, contributing to its stabilization upregulation. Consequently, activated Nrf2/GPX4 axis, resulting increased GPX4 expression, inhibition GPX4-mediated facilitation progression. Our findings underscore clinical relevance illuminate regulatory suggesting implications targeted precision medicine

Language: Английский

Citations

0