KM-Survival Analysis is depicted through Hazard Ratio (HR) and p-value identification. Drug-Target Docking Analysis of ligand molecule Hyaluronic Acid and drugs 5-Fluorouracil and Epirubicin and TCGA Drug Survival Analysis and Response are implicated for therapeutic interventions.
It provides insights into the molecular mechanisms underlying UDA's anti-cancer properties and its potential as a therapeutic agent targeting HA signaling in cancer. Further research is needed to elucidate these mechanisms and explore UDA's clinical applications.
In surgical specimens, miR-10a expression was higher in PC compared to Benign Prostatic Hyperplasia (p = 0.0010). Increased expression of miR-10a affects cell migration, invasion, and proliferation, showing potential as a therapeutic target in treating PC.
These findings indicate that HPV integration drives transcriptional activation near ISs, enhancing expression of adjacent oncogenes. Our study deepens understanding of HPV-induced carcinogenesis and informs precision medicine strategies for cervical cancer.
Whole-exome sequencing revealed two candidate single-nucleotide polymorphisms: HAS3 rs2232228 and RAC2 rs13058338, which may be implicated in the genetic predisposition to anthracycline-related cardiomyopathy. This case highlights the importance of considering early-onset cardiotoxicity in pediatric patients and supports further research into genetic risk-based screening and prevention strategies.
5 months ago
Journal
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HAS3 (Hyaluronan Synthase 3) • RAC2 (Rac Family Small GTPase 2)
The same result was observed in co-culture experiments involving INS-1E cells and stromal vascular fraction (SVF) from adipose tissue. These experiments aim to investigate the effects of 4MU on beta cells in the context of its potential use in early-stage type 1 diabetes and in enhancing islet transplantation outcomes.
Importantly, silencing CD44 expression in MM cells reduced F-actin polymerization, as well as impaired MM cell migration and adhesion to HS5. Our findings highlight the involvement of the HA/CD44/F-actin pathway in MM-BM migration and adhesion, suggesting that CD44 may serve as a novel therapeutic target to disrupt the MM-BM microenvironment.
For methotrexate, the genes ABCC2, MTHFR, and SXR were associated with myelosuppression and hepatotoxicity...This review highlights the complexity and variability of pharmacogenomic associations with chemotherapy-induced toxicities in pediatric oncology. While certain genetic variants show associations with specific toxicities, larger multinational/center studies are needed to strengthen the associations and improve clinical guidelines.
11 months ago
Review • Journal
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ERCC2 (Excision repair cross-complementation group 2) • GSTP1 (Glutathione S-transferase pi 1) • MTHFR (Methylenetetrahydrofolate Reductase) • ABCC2 (ATP Binding Cassette Subfamily C Member 2) • ABCB4 (ATP Binding Cassette Subfamily B Member 4) • ABCC3 (ATP Binding Cassette Subfamily C Member 3) • GSTM1 (Glutathione S-transferase mu 1) • HAS3 (Hyaluronan Synthase 3) • RARG (Retinoic Acid Receptor Gamma) • GSTT1 (Glutathione S-transferase theta 1) • SLC22A2 (Solute Carrier Family 22 Member 2) • SLC28A3 (Solute Carrier Family 28 Member 3) • CELF4 (CUGBP Elav-Like Family Member 4) • COMT (Catechol-O-Methyltransferase)
Using a deep learning-based drug-target interaction algorithm, we identified an ITIH2 inhibitor (sincalide) that inhibited HA matrix formation and migration of lung cancer cells, preventing metastatic colonization of lung cancer cells in mouse models. These findings suggest that ZEB1 remodels the HA network in the TME through the regulation of ITIH2, HAS2, and CD44, presenting a strategy for targeting this network to suppress lung cancer progression.
Furthermore, NK‑CdM inhibited the UVB‑induced reduction in the levels of these proteins. Overall, these findings suggested that NK‑CdM has the potential to prevent UVB‑mediated photoaging and promote skin health.
The HA synthesis inhibitors reduced steatotic liver-associated metastasis of colorectal cancer, YAP expression, CAF and M2 macrophage infiltration. In conclusion, steatotic liver modulates a fibrotic tumor microenvironment to enhance metastatic cancer activity through a bidirectional regulation between CAFs and metastatic tumors, enhancing the metastatic potential of colorectal cancer in the liver.
Bexarotene potentially exerts its anti-tumor effect by reducing HA levels through decreased expression of HAS. These findings provide new insights into the process of CTCL development and additional insights regarding bexarotene treatment.