Non-small cell lung cancer (NSCLC) is a highly prevalent and aggressive malignancy, where early diagnosis and therapeutic intervention are pivotal for enhancing patient prognosis. Nonetheless, the lack of reliable biomarkers remains a substantial hurdle in clinical practice. In this study, we identified dysregulated microRNAs (miRNAs) in NSCLC, revealing a significant downregulation of miR-3202 and an upregulation of miR-3182. We demonstrate that both miR-3202 and miR-3182 play critical roles in modulating NSCLC cell proliferation and motility. Notably, we identify DTL as a direct target of miR-3202, with sustained expression of DTL reversing the effects of miR-3202 on cell growth and migration. Mechanistically, we show that miR-3202 regulates the ubiquitination and proteasomal degradation of p21 through DTL. These findings provide novel insights into the miRNA landscape in NSCLC and underscore the functional significance of the miR-3202-DTL-p21 axis. Our results position miR-3202 as a potential biomarker for NSCLC, thereby offering a foundation for the development of targeted diagnostic and therapeutic strategies.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s11010-025-05239-6 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
SOS1 inhibitor BI-3406 shows in vivo antitumor activity akin to genetic ablation and synergizes with a KRAS inhibitor in KRAS LUAD.
Proc Natl Acad Sci U S A
March 2025
Laboratorio 1. Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas-Universidad de Salamanca and Centro de Investigación Biomédica en Red Cáncer (CIBERONC), Salamanca 37007, Spain.
We evaluated the in vivo therapeutic efficacy and tolerability of BI-3406-mediated pharmacological inhibition of SOS1 in comparison to genetic ablation of this universal Ras-GEF in various KRAS-dependent experimental tumor settings. Contrary to the rapid lethality caused by SOS1 genetic ablation in SOS2 mice, SOS1 pharmacological inhibition by its specific inhibitor BI-3406 did not significantly affect animal weight/viability nor cause noteworthy systemic toxicity. Allograft assays using different KRAS cell lines showed that treatment with BI-3406 impaired RAS activation and RAS downstream signaling and decreased tumor burden and disease progression as a result of both tumor-intrinsic and -extrinsic therapeutic effects of the drug.
View Article and Find Full Text PDFLeukemogenic Kras mutation reprograms multipotent progenitors to facilitate its spread through the hematopoietic system.
J Exp Med
June 2025
Department of Pathology, New York University Grossman School of Medicine, New York, NY, USA.
Leukemia-driving mutations are thought to arise in hematopoietic stem cells (HSC), yet the natural history of their spread is poorly understood. We genetically induced mutations within endogenous murine HSC and traced them in unmanipulated animals. In contrast to mutations associated with clonal hematopoiesis (such as Tet2 deletion), the leukemogenic KrasG12D mutation dramatically accelerated HSC contribution to all hematopoietic lineages.
View Article and Find Full Text PDFBreaking Barriers; Phytoestrogens in the Fight Against Triple-Negative Breast Cancer: A Comprehensive Review.
Med Res Rev
March 2025
Biochemistry and Molecular Biology, Primeasia University, Banani, Dhaka, Bangladesh.
The development of standard drugs for some unusual cancers, including estrogen-nonresponsive breast cancer, is somewhat difficult within a very short time. So, considering the current situation, phytoestrogen may be a potential candidate for unraveling chemotherapeutics agents. The reason for this review article is to manifest overall information regarding the effects of phytoestrogen on triple-negative breast cancer (TNBC), along with its related cellular and molecular pathways in different TNBC models.
View Article and Find Full Text PDFRegulates Muscle Growth and Development by Targeting .
Cells
March 2025
Key Laboratory of Swine Genetics and Breeding of the Ministry of Agriculture and Rural Afairs, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, China.
Non-coding genes, such as microRNA and lncRNA, which have been widely studied, play an important role in the regulatory network of skeletal muscle development. However, the functions and mechanisms of most non-coding RNAs in skeletal muscle regulatory networks are unclear. This study investigated the function and mechanism of in muscle growth and development.
View Article and Find Full Text PDFA Cross-Sectional Exploratory Study of Rat Sarcoid (Ras) Activation in Women with and Without Polycystic Ovary Syndrome.
Cells
March 2025
Research Department, Royal College of Surgeons of Ireland, Busaiteen, Adliya P.O. Box 15503, Bahrain.
: Rat sarcoma (Ras) proteins, Kirsten, Harvey, and Neuroblastoma rat sarcoma viral oncogene homolog (KRAS, HRAS, and NRAS, respectively), are a family of GTPases, which are key regulators of cellular growth, differentiation, and apoptosis through signal transduction pathways modulated by growth factors that have been recognized to be dysregulated in PCOS. This study explores Ras signaling proteins and growth factor-related proteins in polycystic ovary syndrome (PCOS). : In a well-validated PCOS database of 147 PCOS and 97 control women, plasma was batch analyzed using Somascan proteomic analysis for circulating KRas, Ras GTPase-activating protein-1 (RASA1), and 45 growth factor-related proteins.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!