SPINK1 overexpression

FOXM1 directly promotes SPINK1 transcription, enhancing tumor cell proliferation and metastasis while regulating the p53 pathway. Targeting this axis could provide a potential therapeutic approach for liver cancer.

Experimental evidence further demonstrates that SPINK1 overexpression induces the expression of CES2 and CYP3A5, consequently promoting chemoresistance to sorafenib and oxaliplatin. In summary, our study unveils the predictive role of SPINK1 on HCC treatment resistance, identifying it as a potential therapeutic target for refractory HCC.

Enhanced transcriptional activity of SPINK1 is mediated by promoter binding of ELF3, which like CD133, is found to increase following 5-FU and cisplatin treatment; while targeted depletion of CD133 will reduce both ELF3 and SPINK1...Depleting SPINK1 function by neutralizing antibody treatment or in vivo lentivirus-mediated Spink1 knockdown dampens HCC cancer growth and their ability to resist chemotherapy. Targeting oncofetal SPINK1 may represent a promising therapeutic option for HCC treatment.

Furthermore, the study revealed associations between CKD stages and prognostic grade groups in different molecular subtypes, pointing out an intricate interplay between renal function and tumor behavior. Although the molecular classification of prostate acinar ADK is not yet implemented, this research underscores the variability of renal function parameters in different molecular subtypes, offering potential insights into patient prognosis.

Chloroquine (CQ) significantly decreased the level of autophagy in both control and SPINK1-OE HT29 cells...Collectively, SPINK1-promoted proliferation and clonal formation of HT29 cells were closely associated with Beclin1 associated enhanced autophagy. The above findings would open a new window for probing the role of SPINK1-related autophagic signaling in the pathogenesis of CRC.

Especially, prostate-specific genes, PSA and PSMA, were highly detectable and expressed at metastatic PCa.ConclusionOur data showed that considerable selected genes were overexpressed at metastatic PCa. Transcriptomic analysis via CTC-based multigene profiling may guide the early diagnosis of advanced PCa and provide an additional means of risk stratifying PCa.

We studied five classifiers that identify subtypes of prostate tumors and found that subtypes differed in frequency between Black and White patients. Further research is warranted to evaluate how differences in tumor subtypes may contribute to disparities in prostate cancer mortality.

We found an interesting finding that the 73-03 in combination with GCB can improve GCB efficacy and decrease PCa resistance, which induced apoptosis and mitochondrial damage through epigenetic inhibition of SPINK1 transcription by miR-421 up-regulation. This was the first study that used OA derivatives on GCB-resistant PCa cells, so this combined strategy warrants further investigation.

Serum SPINK1 had a high diagnostic efficacy for predicting HBV-related HCC. The presence of HBV-related HCC with a high serum SPINK1 level (≥ 2.48 ng/mL) may be associated with a poor short-term prognosis.