Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 260, P. 155408 - 155408
Published: June 13, 2024
Language: Английский
Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 260, P. 155408 - 155408
Published: June 13, 2024
Language: Английский
Clinical and Experimental Medicine, Journal Year: 2025, Volume and Issue: 25(1)
Published: Feb. 11, 2025
Overcoming cancer and enhancing patient survival are becoming increasingly challenging due to the uncontrolled growth metastasis of colorectal cells. In order provide effective treatment minimize malignancy cells, it is necessary understand how complex signaling networks contribute their invasion proliferation. The signal transducer activator transcription 3 (STAT3) a promising target its involvement in various cellular functions, including apoptosis, immunosuppression, cell invasion, migration, Dysregulation STAT3 associated with diseases, particularly cancer. Long non-coding RNAs (lncRNAs), subset RNAs, essential for progression, CRC as they regulate key pathways such gene regulation at epigenetic, transcriptional, post-transcriptional levels. Moreover, lncRNAs have function regulating immune cells through STAT3. this study, we comprehensively reviewed regulatory roles different on mutual effects pathway aspects carcinogenesis, proliferation, metastasis, drug resistance, angiogenesis. investigate lncRNA/STAT3 axis that play critical role tumor microenvironment.
Language: Английский
Citations
0International Journal of Innovations in Science Engineering and Management., Journal Year: 2025, Volume and Issue: unknown, P. 174 - 180
Published: Feb. 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.
Language: Английский
Citations
0Archives of Physiology and Biochemistry, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 13
Published: March 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.
Language: Английский
Citations
0Research, Journal Year: 2025, Volume and Issue: 8
Published: Jan. 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
Language: Английский
Citations
0Discover Oncology, Journal Year: 2025, Volume and Issue: 16(1)
Published: March 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.
Language: Английский
Citations
0Journal 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
0Gene, Journal Year: 2025, Volume and Issue: unknown, P. 149433 - 149433
Published: March 1, 2025
Language: Английский
Citations
0Journal of Biochemical and Molecular Toxicology, Journal Year: 2025, Volume and Issue: 39(4)
Published: March 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.
Language: Английский
Citations
0Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16
Published: April 24, 2025
As a highly prevalent gastrointestinal malignant tumor, colorectal cancer poses serious challenge in terms of increasing morbidity and mortality late diagnosis due to the invisibility disease. Although existing therapies are diverse but limited efficacy, mechanism programmed cell death (PCD) has become focus research its central role maintaining body homeostasis regulating tumor progression. Multimodal pathways, such as apoptosis, autophagy, pyroptosis ferroptosis, have shown unique advantages inhibiting proliferation migration cells enhancing sensitivity chemotherapy by responding internal external environmental stimuli. In recent years, natural products risen prominence virtue their multi-target synergistic effects chemo-sensitizing properties, opened up new direction for treatment precisely PCD pathway. this paper, we searched PubMed, Web Science CNKI databases relevant studies last 10 years using keywords (Colorectal cancer) (programmed death) products. This work retrieved 59 (55 from past 5 4 years) reveal action targeting PCD, aiming provide theoretical support practical guidance optimization clinical therapeutic strategies development innovative drugs.
Language: Английский
Citations
0Journal of Cellular and Molecular Medicine, Journal Year: 2025, Volume and Issue: 29(9)
Published: May 1, 2025
ABSTRACT Existing knowledge regarding the involvement of lncRNA OIP5 ‐ AS1 in lung adenocarcinoma ( LUAD ) development is still incomplete and requires further investigation. Our research aimed to reveal function . We evaluated level its association with clinicopathological factors The examined potential implications targeting mitigating invasive properties cancer cells. A nude mouse xenograft model was utilised examine tumour growth. used bioinformatics data a dual‐luciferase reporter assay study interactions between hsa‐ miR ‐29b‐3p. significantly overexpressed , higher correlating adverse features. Knockdown resulted notable decreases cell growth, movement, aggressive behaviour, accompanied by decrease size vivo. Furthermore, confirmed act as molecular sponge for elevated expression ‐29b‐3p intensified inhibitory outcomes knockdown on properties. ZIC5 experimentally determined be direct target hs‐ ‐29b‐3p, emphasising integral position regulatory interaction. This reveals new route involving pathogenesis. Given oncogenic traits, presents promising predictive biomarker therapeutic optimising treatment.
Language: Английский
Citations
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