SLC8A1 (Solute Carrier Family 8 Member A1)

Conclusions Based on bioinformatical approaches, we identified significantly enriched gene sets and novel candidates for prognostic markers or therapeutic targets in HNSCC. Further investigation would aid in determining the anti-cancer effects of these candidates.

Additionally, when combining positive ß-catenin expression and sequencing results, the aberrant/mutant CTNNB1 gene was shown in three tumors (75% of analyzed cases) in this IPM series. The present data provides additional support/adjunct to establish the rare diagnosis of intranodal palisaded myofibroblastomas with amianthoid fibers by molecular testing in diagnostically challenging cases.

The relationship between DNA methylation and gene expression is complex. Plasma-based DNA methylation markers can effectively discriminate between IPA and NPA, as well as between NPA and healthy individuals (N group).

Low SPIN1 expression group could benefit from Axitinib, Cytarabine, Pazopanib and Sunitinib. Finally, we screened the 10 genes with the strongest correlation with SPIN1, among which CDH11 and SLC8A1 were associated with the prognosis of GC. In conclusion, our study has provided valuable insights into the pivotal role of SPIN1 in GC development, elucidating its potential molecular mechanisms and establishing it as a promising therapeutic target.

Furthermore, ATF3, GJA1, JPH2, MVB12B, RUNX1T1, SLC8A1, SPATA6, and TPM3 may be potential target genes of these three miRNAs. We developed a three-miRNA panel that could serve as a highly efficient and inexpensive biomarker for BC diagnosis and screening.

We demonstrated that SLC8A1 selective pharmacological inhibition, through CB-DMB, significantly reduced cancer proliferation and induced Ca2+-dependent cell death in GC cells, both alone and synergically with cisplatin treatment. SLC8A1 inhibition could represents a potential subgroup-specific therapeutic approach for GC patients based on its ability to induce Ca2+-dependent cell death.

We provide robust causal evidence for prioritising genes and their protein products in glioma research. Our results highlight the importance of alternative splicing as a mechanism in gliomagenesis and as an avenue for exploration of drug targets.

In vitro loss-of-function cell-based assays and in vivo experiments using three CRC cell lines with different metastatic properties assessed the important roles of SLC8A1 and TXNDC17 in CRC and liver metastasis. Additionally, SLC8A1 and TXNDC17 protein levels in plasma possessed the diagnostic ability of early CRC stages.

Prediagnostic ctDNA markers are promising contributors to predicting poor prognosis in CRC, potentially becoming one of the tools guiding more personalised treatment.

Patients classified in the low-risk group exhibited enhanced responsiveness to osimertinib, dasatinib, and ibrutinib. The results of in vitro experiments revealed that SLC8A1 promotes proliferation and inhibits the apoptosis and concentration of calcium ions in HTR-8/SVneo cells. These findings suggest that SLC8A1 may serve as a promising prognostic biomarker and potential target for immunotherapy in the context of RSA and UCEC.

We established a risk model with ERS-related genes (PMM2, STC2, EIF2AK1, HSPA1A, SLC8A1, KCNQ1), which enhance the sensitivity of immunotherapy for colon cancer. These may provide a new perspective for the treatment of colon cancer.