SLC22A3 (Solute Carrier Family 22 Member 3)

Further research is needed on PPI and benign gastrointestinal diseases. Our multi-omics integration reveals tissue-specific PPI pharmacodynamics, identifying targets with dual therapeutic/carcinogenic potential that may explain epidemiological discordances.

NUCKS1 was expressed in each cell type and was lower in T/NK and NK cells. The study deepens the understanding of PAH pathogenesis, and may provide diagnostic targets for PAH.

Additionally, the hormone-mediated upregulation and AR antagonist-driven downregulation of PSA gene expression were respectively attenuated and enhanced in PACT KO cells. Taken together, these data support a pro-proliferative role for PACT in PCa, and siRNA therapeutic targeting of PACT, or downregulated genes with PACT KO, could represent a new therapeutic approach.

Our study elucidates the predictive versus prognostic effect of metabolic pathways in advanced NSCLC under immunotherapy. Tumor-intrinsic carnitine metabolism may predict and drive immunotherapy resistance, and targeting SLC22A5-mediated carnitine metabolism could be used to overcome resistance in advanced NSCLC.

SLC22A3 acts as protective factor in breast cancer. Enhanced m6A methylation of SLC22A3 mRNA and overexpression of the m6A reader IGF2BP2 upregulate its expression. The induction of SLC22A3 mRNA methylation through the m6A CRISPR approach effectively mitigates the malignancy of breast cancer cells.

Finally, a binary logistic model based on cytidine deaminase (CDA) and solute carrier family 22 member 7 (SLC22A7) was constructed for early-warning of diarrhea induced by Cap: Y = 0.028 × CDA (pg/mL) - 0.518 × SLC22A7 (pg/mL) + 1.526, with the area under curve of 0.907 (specificity 100.0%, sensitivity 71.4%) for diarrhea CRC patients. This study constructed and validated, for the first time, an early-warning model of diarrhea caused by Cap based on metabolic enzymes and drug transporters in normal colon tissue, which may provide a new basis for accurate medication for CRC treatment in clinical practice.

The present study identified circSLC22A3 as a new tumor suppressor that inhibited ESCC progression through both the circSLC22A3/ miR-19b-3p/ TRAK2 and circSLC22A3/ IGF2BP1/ ACSBG1 axes.

(4) Our findings highlight the potential of using this SNP as a biomarker for predicting chemotherapeutic outcomes and uncover possible mechanisms underlying drug resistance in advanced prostate cancers. More importantly, it provides a clinical foundation for targeting FOXA1 to enhance drug efficacy in prostate cancer patients.

The SLC22A17 methDNA hotspot could represent a promising biomarker for CM, highlighting the regulatory role of methDNA on SLC22A17 expression. These results pave the way for the identification of novel epigenetic biomarkers and therapeutic targets for the management of CM patients.

These results show that canine CPs exhibit the expression of surrogate markers that suggest sensitivity to metformin, such as upregulated OCT3 and pS6 expression. Taken together, these findings provide the rationale for the early assessment of the use of metformin as a mechanism-based therapeutic approach for treating canine patients with persistent or multiple CPs.

Ectopic expression of GRHL3 or SLC22A31 abated the suppressing impact of ZNF217 or GRHL3 knockdown on the biological activity of THCA cells. Collectively, our results demonstrated that ZNF217 acted as an activator of GRHL3, thereby promoting the expression of SLC22A31 and the malignant activity of THCA cells.

In contrast, hsa-miR-650 is involved in the regulation of HTR6 expression, whereas hsa-miR-1275 potentially interacts with three mRNAs: ADA, SLC23A2, and HRH1. Molecular analysis confirmed that the selected mRNA and miRNA transcripts could be promising molecular markers and therapeutic targets.