ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1)

Serum concentrations of ALCAM and ALDH1 were significantly elevated in our patient cohort with rectal cancer but showed no significant correlation with tumor stage or survival, whenever serum samples were obtained either during or after neoadjuvant and adjuvant therapy, which may be particularly due to the limited number of studied subjects. Although their prognostic utility remains limited, their consistent elevation in cancer patients underscores their potential value in early detection or as components of a broader biomarker panel.

The immunolabeling method produced consistent results for this group of enzymes, which might lead to successful application in predicting tumor prognosis. Other NADPH-related enzymes, such as glutamate dehydrogenase (GDH), aldehyde dehydrogenase 1 (ALDH1), and dihydrofolate reductase (DHFR), deserve more extensive investigation to elucidate their potential as cancer biomarkers via IHC.

Cell counting kit-8 (CCK-8) assay, 5-Ethynyl-2'-deoxyuridine (EdU) assay, colony formation assay and Annexin V-FITC/PI assay were performed to detect the anti-cancer effects of HQD and EGFR-TKIs (1st generation EGFR-TKI gefitinib or 3rd generation EGFR-TKI Osimertinib) in different NSCLC cell lines. Moreover, the drug safety, anti-cancer effect and potential mechanism of the therapy of HQD and EGFR-TKIs were confirmed in vivo. HQD enhances the anti-cancer effect of EGFR-TKIs in NSCLC through ROS-mediated CSC makers inhibition by suppressing stat3/GPX4 axis to induce redox ratio, providing a novel strategy for the treatment of NSCLC patients.

This article ultimately provides a foundation for researchers to further investigate these interconnected processes and for clinicians to consider therapeutic strategies when managing patients with lung cancer. Given the multifaceted nature of lung cancer biology and the numerous molecules involved, we advocate for a panel-centered approach in both research and clinical management, while underscoring the importance of carefully considering toxicity risks and variability in molecular expression.

Functional studies established that E2F2 directly regulates FZD10 expression, activating the Wnt/β-catenin pathway to sustain the stem-like state. Collectively, we unveil the E2F2/FZD10 axis as a previously unrecognized molecular conduit through which environmental arsenic reprograms mammary epithelial cells toward a BCSCs-like phenotype, providing mechanistic insight into arsenic-associated breast cancer risk and revealing a potential target for preventive intervention.

These findings demonstrated that ebastine effectively disrupts key pathways involved in CSC‑like traits and HER2 activity, even under trastuzumab‑resistant conditions. Its multifaceted inhibitory effects support the repositioning of ebastine as a promising therapeutic strategy for treating refractory HER2‑positive breast cancer.

Taken together, these findings illustrated that OSBPL2-mediated lipid transportation inhibited the stemness and aggressiveness of lung cancer cells. OSBPL2 was a potential therapeutic target to develop novel cancer-preventive compound.

The compensatory expression of Twist1 in FOXP2-overexpressing breast cancer cells counteracted FOXP2's inhibitory effects on the stemness of breast cancer cells. Together, the results showed that FOXP2 attenuated the stemness of breast cancer cells by abolishing the transcription of Twist1.

Pan-cancer analysis revealed the potential of ZNF184 as a prognostic and predictive biomarker for adverse clinical outcomes. Collectively, these findings reveal a previously unknown role of ZNF184 in breast cancer progression and paclitaxel resistance, providing new insights into ZNF184 as a potential therapeutic target for cancer patients.

Increased metastatic potential was also confirmed in HT-29 cells after ALDH1A1 genetic attenuation. CRISPR-Cas9-mediated editing led to functional, cellular, and molecular changes confirming the role of ALDH1A1 in colorectal cancer carcinogenesis.

Mechanistically, USP30-AS1 acts as a competing endogenous RNA (ceRNA) by sponging miR-3646, which leads to the derepression of Frizzled-7 (FZD7) and subsequent activation of the Wnt/β-catenin signaling pathway. These findings identify USP30-AS1 as a critical promoter of stemness, chemoresistance, and metastasis in BCSCs via the miR-3646/FZD7/Wnt axis, suggesting it is a potential therapeutic target for breast cancer intervention.

This study reveals the prognostic metabolic pathways and important prognostic target genes in BCBM from the perspective of metabolism-immunity interaction. MRGs can well distinguish the prognosis of different patients, and metabolism-related risk modeling can be used as a good prognostic predictor, which provides valuable insights into the "metabolic-immune" perspective of treatment.