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

Pathology - Research and Practice, Год журнала: 2025, Номер 266, С. 155810 - 155810

Опубликована: Янв. 5, 2025

Язык: Английский

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Elevated LINC00115 expression correlates with aggressive endometrial cancer phenotypes via JAK/STAT pathway modulation

Human Molecular Genetics, Год журнала: 2025, Номер unknown

Опубликована: Янв. 7, 2025

Abstract This study systematically explores the oncogenic role of long non-coding RNA (lncRNA) LINC00115 in endometrial cancer (EC) and reveals its unique mechanism promoting proliferation, invasion, metastasis via JAK/STAT signaling pathway. is significantly upregulated EC tissues closely associated with advanced TNM staging lymph node metastasis. Functional assays showed that knockdown suppressed cell metastasis, while overexpression enhanced these malignant behaviors. In vivo models confirmed accelerates tumor growth Our first to identify as a key activator pathway through direct interaction KH-type Splicing Regulatory Protein (KHSRP), previously unrecognized EC. finding provides new insights into lncRNA-mediated regulation highlights novel biomarker promising therapeutic target for EC, offering theoretical basis developing targeted therapies.

Язык: Английский

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TFAP2A Activates ADAM8 to Promote Lung Adenocarcinoma Angiogenesis Through the JAK/STAT Signaling Pathway

Journal of Biochemical and Molecular Toxicology, Год журнала: 2025, Номер 39(1)

Опубликована: Янв. 1, 2025

As the most prevalent subtype of lung cancer, adenocarcinoma (LUAD) is closely associated with angiogenesis, which fundamental to its progression. ADAM8 (A disintegrin and metalloproteinase 8) an enzyme tumor invasion, while implications in LUAD angiogenesis are a field that awaits exploration. A thorough investigation into impacts on could contribute development therapeutic drugs for LUAD. Bioinformatics delineated expression profiles TFAP2A tissues, focusing ADAM8-enriched pathways. qRT-PCR confirmed their cells. The CCK-8 assay was applied gauge cell viability, Western blot detected presence JAK2/STAT3 pathway proteins VEGFR-2 VEGF. Angiogenesis assays quantified length dual-luciferase Chromatin immunoprecipitation verified TFAP2A-ADAM8 binding. exhibited high tissues cells, notable enrichment VEGF JAK/STAT Cellular revealed elevated enhanced promoted phosphorylation JAK2 STAT3, boosted angiogenic capacity. JAK inhibitor Peficitinib reversed proangiogenic effects induced by overexpression. We also discovered overexpression TFAP2A, upstream transcription factor ADAM8, Rescue experiments indicated counteract inhibitory knockdown angiogenesis. This study reveals first time critical role demonstrating promotes conduction activating ADAM8. finding not only provides new perspective understanding pathogenesis but lays foundation therapies targeting

Язык: Английский

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The Role of Non-Coding RNAs in Gene Regulation and Cellular Signaling Pathways

International Journal of Innovations in Science Engineering and Management., Год журнала: 2025, Номер unknown, С. 174 - 180

Опубликована: Фев. 22, 2025

Evidence has been mounting over the last decade demonstrating crucial functions of ncRNAs, including miRNAs and long non-coding RNAs (lncRNAs), in cellular signalling networks gene regulation. These ncRNAs are highly expressed play a role regulating processes metastasis endothelial cell invasiveness. They facilitate crosstalk between interconnected signaling pathways, PTEN/PI3K/AKT/mTOR, by acting as linking molecules within signal circuits. In addition to expression conventional apical measures, studying provides better understanding both beneficial detrimental reactions external exposures. Additionally, miRNAs—which may be found extracellular intracellular environments, such biofluids—have become potential early precise molecular indicators tissue conditions. This review highlights regulatory their involvement homeostasis, biomarkers, shedding light on significance regulation, toxicological studies, precision medicine.

Язык: Английский

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Tumour protein p53-activated lncRNA PGM5-AS1 suppresses lung cancer growth and stemness by targeting R-spondin1 via microRNA-1247-5p

Archives of Physiology and Biochemistry, Год журнала: 2025, Номер unknown, С. 1 - 13

Опубликована: Март 4, 2025

This study was to investigated the inhibitory role of tumour protein p53 (TP53)-activated PGM5-AS1 in lung cancer (LC) cell proliferation, invasion, and CSC-like properties its underlying mechanisms. The effect on LC development determined. Stem markers, aldehyde dehydrogenase activity cells were tested, as well ability stem form spheroids. interaction TP53 binding link PGM5-AS1, miR-1247-5p, R-spondin1 (RSPO1) verified. elevated by a combination promoters. molecular sponge miR-1247-5p cells, targeted RSPO1. Elevating or repressing restrained growth stemness, which reversed depression conveys that TP53-elevated mediates target RSPO1, thereby inhibiting representing novel avenue for therapy.

Язык: Английский

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EGF-upregulated lncRNA ESSENCE promotes colorectal cancer growth through stabilizing CAD and ferroptosis defence

Research, Год журнала: 2025, Номер 8

Опубликована: Янв. 1, 2025

Epidermal growth factor receptor/mitogen-activated protein kinase (EGFR/MAPK) signaling is highly activated in various types of cancer. The long noncoding RNAs induced by this pathway and their roles colorectal cancer (CRC) have not been fully elucidated. In study, based on the profiling triggered EGFR/MAPK signaling, we identified that ESSENCE (EGF [epidermal factor] Signal Sensing CAD’s Effect; ENST00000415336), which mediated transcription early response 1, functions as a potent oncogenic molecule predicts poor prognosis CRC. Mechanistically, directly interacts with carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, dihydroorotase (CAD) competitively attenuates CAD degradation its newly discovered E3 ligase KEAP1, thereby suppressing ferroptosis promoting CRC progression. Importantly, combinational treatment mitogen-activated extracellular signal-regulated inhibitor selumetinib inducer sulfasalazine synergistically suppresses ESSENCE-high patient-derived xenograft mouse model. Taken together, these findings demonstrate crucial role mediating progression regulating stabilization suggest therapeutic strategy targeting ESSENCE–CAD axis

Язык: Английский

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ESM1 suppresses LncRNA GAS5/miR-23a-3p/PTEN axis to promote the cisplatin-chemotherapy resistance of ovarian cancer cells via activating the PI3K/AKT pathway

Discover Oncology, Год журнала: 2025, Номер 16(1)

Опубликована: Март 16, 2025

Cisplatin chemotherapy is an important treatment for advanced ovarian cancer (OC). However, the development of cisplatin resistance greatly limits survival time OC patients. Endothelial cell-specific molecule 1 (ESM1) has been found to be proto-oncogene promoting OC, but its mediating remains unknown. We used quantitative polymerase chain reaction (qPCR) measure transcription levels ESM1, Growth arrest specific transcript 5 (GAS5), miR-23a-3p, and Phosphatase And Tensin Homolog (PTEN). A double luciferase reporter gene assay confirmed direct binding GAS5 miR-23a-3p PTEN mRNA. The effects GAS5, on were tested with Half Maximal Inhibitory Concentration (IC50) assay. Flow cytometry was assess cisplatin-induced apoptosis. Changes in apoptosis-related proteins PI3K/AKT-related analyzed western blot (WB). ESM1 inhibits increases miR-23a-3p. promote resistance. sensitivity cells. Moreover, main molecular mechanism ESM1/GAS5/miR-23a-3p/PTEN/PI3K/Akt signaling axis. promotes by activating Phosphoinositide-3-Kinase (PI3K)/AKT Serine/Threonine Kinase (Akt) pathway through GAS5/miR-23a-3p/PTEN This suggests that prescriptive regulates key downstream mechanisms via non-coding RNA can before neoadjuvant initiated.

Язык: Английский

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LINC00942 Accelerates Esophageal Cancer Progression by Raising PRKDC Through Interaction With PTBP1

Journal of Biochemical and Molecular Toxicology, Год журнала: 2025, Номер 39(3)

Опубликована: Март 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.

Язык: Английский

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Prognostic gene expression profile of colorectal cancer

Gene, Год журнала: 2025, Номер unknown, С. 149433 - 149433

Опубликована: Март 1, 2025

Язык: Английский

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M2 Macrophage‐Extracellular Vesicle‐Derived lncRNA‐NEAT1 Regulates miR‐204‐5p/RRS1‐mediated Cell Cycle to Promote the Occurrence and Development of Colorectal Cancer

Journal of Biochemical and Molecular Toxicology, Год журнала: 2025, Номер 39(4)

Опубликована: Март 31, 2025

ABSTRACT Colorectal cancer (CRC) is a prevalent malignancy of the digestive system. Here, we explored role M2 macrophage‐derived extracellular vesicles (EVs) carrying long non‐coding RNA‐nuclear paraspeckle assembly transcript 1 (lncRNA‐NEAT1) in promoting CRC progression via regulation miR‐204‐5p/regulator ribosome synthesis (RRS1) axis and cell cycle dynamics. Firstly, differentiated WTHP‐1 cells into M0 macrophages transfected with sh‐NEAT1 lentivirus plasmids. EVs were isolated from administered to SW480 along miR‐204‐5p inhibitors or si‐RRS1 for 24 h. M2‐EVs‐derived lncRNA‐NEAT1 enhanced proliferation, migration, invasion, viability while reducing apoptosis. This was accompanied by increased expression RRS1, WEE1 G2 checkpoint kinase (WEE1), cyclin‐dependent (CDK1), CyclinB1, reduced levels, lower proportion G2/M phase. Knockdown reversed these effects. Mechanistically, functioned as competing endogenous RNA (ceRNA), sponging upregulate RRS1 expression. In summary, promote development modulating miR‐204‐5p/RRS1 axis, influencing These findings provide insights tumor‐promoting mechanisms CRC.

Язык: Английский

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