MLC1 Overexpression Inhibits Tumor Progression through PI3K/AKT Signal Pathway in Prostate Cancer

Wu, Zonglin; Ni, Jinliang; Zhang, Houliang; Zhang, Yifan; Lv, Chengxun; Wang, Yidi; Wang, Keyi; Peng, Bo

doi:10.1002/adbi.202300060

Cited by 2 publications

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Genomic Discovery of EF-24 Targets Unveils Antitumorigenic Mechanisms in Leukemia Cells

Singh,

Wax,

Duncan

et al. 2024

Preprint

View full text Add to dashboard Cite

Curcumin, a polyphenolic compound derived from the plantCurcuma longaL., has demonstrated a wide range of therapeutic properties, including potential anticancer effects. However, its clinical efficacy is limited due to poor bioavailability and stability. To overcome these challenges, curcumin analogs like EF-24 have been developed with improved pharmacological properties. In this study, we used whole-transcriptome profiling to identify the genome-wide functional impacts of EF-24 treatment in leukemia cells to improve our understanding of its potential mechanisms of action. This approach allowed us to establish a model system for associating druggable genes with clinical disease targets. We used the chronic myeloid leukemia (CML) cell line K-562 and acute myeloid leukemia (AML) cell lines HL-60, Kasumi-1, and THP-1 to conduct EF-24 treatment studies. Cell viability was significantly decreased in the EF-24treated cells as compared to the untreated controls. We discovered that the genes ATF3, CLU, HSPA6, OSGIN1, ZFAND2A, and CXCL8, which are associated with reduced cell viability and proliferation, were consistently upregulated in all EF-24treated cell lines. Further analysis of the tested cell lines revealed the activation of various signaling pathways, including the STAT1 regulated S100 family signaling pathway, that controlled downstream gene expression in response to EF-24 treatment. Our results elucidate the molecular mechanisms underlying EF-24's antitumor efficacy against leukemia, highlighting its multifaceted impact on signaling pathways and gene networks that regulate cell survival, proliferation, and immune responses in myeloid leukemia cells.

show abstract

Genomic Discovery of EF-24 Targets Unveils Antitumorigenic Mechanisms in Leukemia Cells

Singh,

Wax,

Duncan

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

The causal nexus between diverse smoking statuses, potential therapeutic targets, and NSCLC: insights from Mendelian randomization and mediation analysis

Cao,

Zhao,

et al. 2024

Front. Oncol.

View full text Add to dashboard Cite

ObjectiveLung cancer, the most prevalent malignancy, is typically diagnosed at an advanced stage. Smoking is a pivotal risk factor for NSCLC, yet the impact of various smoking statuses on NSCLC remains unclear. Thus, this study aims to explore whether different smoking statuses can causally influence NSCLC through effects on predictive targets, offering a novel perspective for NSCLC treatment.MethodsEmploying dual-sample MR, MVMR, and TSMR approaches, we assessed the causal relationships between 13 distinct smoking statuses and NSCLC, using predicted potential therapeutic targets as mediators to further elucidate the causal interplay among them.ResultsAmong the 13 smoking statuses, current tobacco smoking, exposure to tobacco smoke outside the home, past tobacco smoking, and never smoked demonstrated causal relationships with NSCLC. MVMR analysis reveals that Current tobacco smoking is an independent risk factor for NSCLC. Utilizing NCAPD2, IL11RA, and MLC1 as mediators, IL11RA (22.2%) was found to potentially mediate the relationship between past tobacco smoking and NSCLC.ConclusionThis study, integrating bioinformatics and MR analysis, identified three potential predictive targets as mediators to investigate the causal relationships between different smoking statuses and NSCLC through potential therapeutic targets, providing new insights for the treatment and prevention of NSCLC.

show abstract

MLC1 Overexpression Inhibits Tumor Progression through PI3K/AKT Signal Pathway in Prostate Cancer

Cited by 2 publications

References 23 publications

Genomic Discovery of EF-24 Targets Unveils Antitumorigenic Mechanisms in Leukemia Cells

Genomic Discovery of EF-24 Targets Unveils Antitumorigenic Mechanisms in Leukemia Cells

The causal nexus between diverse smoking statuses, potential therapeutic targets, and NSCLC: insights from Mendelian randomization and mediation analysis

Contact Info

Product

Resources

About