DLD (Dihydrolipoamide Dehydrogenase)

3T3 cells were treated long-term with fluorouracil (5-FU), irinotecan (CPT-11), or cisplatin (CDDP) to generate 3T3-5FU, 3T3-CPT11, and 3T3-CDDP cells, respectively. Pharmacological modulation of LPA signaling further supported receptor-specific effects: the LPA1 antagonist AM966 and the LPA2 agonist GRI-977143 promoted DLD-1 cell growth, while AM966 suppressed and GRI-977143 enhanced cell motility in co-culture with drug-treated fibroblasts. These findings suggest that chemotherapy-conditioned fibroblasts reshape LPA receptor-dependent signaling in colon cancer cells, suggesting potential therapeutic relevance of distinct roles for LPA1 and LPA2 within the drug-modified TME.

These findings suggest that mesalazine differentially modulates DUSP gene expression in normal and malignant colon epithelial cells, potentially contributing to its antiproliferative and pro-apoptotic effects through the regulation of MAPK signaling. These results provide new insights into the molecular mechanisms underlying the anticancer effects of mesalazine in colorectal cancer.

Our findings highlight DLD's predictive value in KIRC and its role in the tumor microenvironment. As a diagnostic and prognostic marker, DLD offers potential for identifying therapeutic targets and enhancing KIRC immunotherapy.

Alirocumab-facilitated 5-FU therapy effectively suppresses PCSK9-promoted CRC proliferation/growth/invasion, highlighting that alirocumab therapy may be an alternative choice of adjuvant therapy in combination with surgery or chemotherapy.

AMIGO2 expression was positively correlated with expression of existing cancer stem cell markers in multiple organ cancer cell lines. These results demonstrate that AMIGO2 accelerates the malignant progression of human cancer cells by inducing a cancer stem cell-like phenotype.

It is concluded that the combination of nonhomologous spectral data fusion would enhance reliability of the single source-derived characteristic markers. The proposed strategy will benefit congeneric researches in the biomedical field.

The combination of HC + 5-FU demonstrated synergistic effects in HT-29 and DLD-1 cells, disrupting oxidative balance and purine metabolism, as reflected in reduced hypoxanthine levels, XOR activity, and ROS production. This treatment also induced mitochondrial membrane depolarisation and altered apoptosis-related gene expression, supporting its role in apoptosis induction.

P=N/A, N=184, Recruiting, University of Cincinnati | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Jun 2026 --> Jun 2027

It has been determined that the compounds eliminate multidrug resistance in breast and colon cancer cells, suppress HSPs and GRPs genes, and lead the cells to death, especially through the antiapoptotic pathway Survivin. These compounds can be evaluated and developed as Survivin inhibitor agents in anticancer studies.

Eb6Mab-3 can detect EphB6 protein in CHO/EphB6 lysate in Western blot. Eb6Mab-3, established by the CBIS method, could be valuable for analyzing the EphB6-associated cellular functions and has potential applications in diagnosis and treatment with specificity and high affinity for cancer cells.

hTERT-RPE1 expressed a p53-responsive transcriptome that was highly representative of diverse experimental systems. We discovered several novel downstream p53 targets of potential clinical relevance including ALDH3A1, which is involved in the detoxification of aldehydes and the metabolism of reactive oxygen species, and nectin cell adhesion molecule 4 (NECTIN4) which encodes a secreted surface protein that is overexpressed in many tumors.

In summary, our research reveals the differential molecular mechanisms of combined PRIMA-1met and L-OHP in CRC with wild type p53 and mutant p53. Our data not only demonstrate that this combined regimen exerts synergistic anti-CRC effect in vitro and in vivo, but also suggest the benefit of PRIMA-1met on prevention of L-OHP-related side effects. These findings underscore the clinical potential of PRIMA-1met-L-OHP combination therapy in CRC, offering enhanced efficacy and reduced toxicity, warranting further clinical investigation.