YB-1 activating cascades as potential targets in KRAS-mutated tumors

Khozooei, Shayan; Veerappan, Soundaram; Toulany, Mahmoud

doi:10.1007/s00066-023-02092-8

Cited by 3 publications

(1 citation statement)

References 236 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…RSK inhibitors, such as LJI308, were designed; however, their long-term use leads to AKT reactivation. As a result, the combination of AKT and RSK inhibitors can be a possible solution and an effective therapeutic strategy [102,103].…”

Section: Yb-1 Inhibitorsmentioning

confidence: 99%

Emerging Therapies in Kirsten Rat Sarcoma Virus (+) Non-Small-Cell Lung Cancer

Karachaliou,

Kotteas,

Fiste

et al. 2024

Cancers

View full text Add to dashboard Cite

Kirsten rat sarcoma virus (KRAS) is the most frequently found oncogene in human cancers, including non-small-cell lung cancer (NSCLC). For many years, KRAS was considered “undruggable” due to its structure and difficult targeting. However, the discovery of the switch II region in the KRAS-G12C-mutated protein has changed the therapeutic landscape with the design and development of novel direct KRAS-G12C inhibitors. Sotorasib and adagrasib are FDA-approved targeted agents for pre-treated patients with KRAS-G12C-mutated NSCLC. Despite promising results, the efficacy of these novel inhibitors is limited by mechanisms of resistance. Ongoing studies are evaluating combination strategies for overcoming resistance. In this review, we summarize the biology of the KRAS protein and the characteristics of KRAS mutations. We then present current and emerging therapeutic approaches for targeting KRAS mutation subtypes intending to provide individualized treatment for lung cancer harboring this challenging driver mutation.

show abstract

Section: Yb-1 Inhibitorsmentioning

confidence: 99%

Emerging Therapies in Kirsten Rat Sarcoma Virus (+) Non-Small-Cell Lung Cancer

Karachaliou,

Kotteas,

Fiste

et al. 2024

Cancers

View full text Add to dashboard Cite

show abstract

A comprehensive view on the fisetin impact on colorectal cancer in animal models: Focusing on cellular and molecular mechanisms

Zamanian,

Taheri,

Ramadan

et al. 2024

Anim Models and Exp Med

View full text Add to dashboard Cite

Flavonoids, including fisetin, have been linked to a reduced risk of colorectal cancer (CRC) and have potential therapeutic applications for the condition. Fisetin, a natural flavonoid found in various fruits and vegetables, has shown promise in managing CRC due to its diverse biological activities. It has been found to influence key cell signaling pathways related to inflammation, angiogenesis, apoptosis, and transcription factors. The results of this study demonstrate that fisetin induces colon cancer cell apoptosis through multiple mechanisms. It impacts the p53 pathway, leading to increased levels of p53 and decreased levels of murine double minute 2, contributing to apoptosis induction. Fisetin also triggers the release of important components in the apoptotic process, such as second mitochondria‐derived activator of caspase/direct inhibitor of apoptosis‐binding protein with low pI and cytochrome c. Furthermore, fisetin inhibits the cyclooxygenase‐2 and wingless‐related integration site (Wnt)/epidermal growth factor receptor/nuclear factor kappa B signaling pathways, reducing Wnt target gene expression and hindering colony formation. It achieves this by regulating the activities of cyclin‐dependent kinase 2 and cyclin‐dependent kinase 4, reducing retinoblastoma protein phosphorylation, decreasing cyclin E levels, and increasing p21 levels, ultimately influencing E2 promoter binding factor 1 and cell division cycle 2 (CDC2) protein levels. Additionally, fisetin exhibits various effects on CRC cells, including inhibiting the phosphorylation of Y‐box binding protein 1 and ribosomal S6 kinase, promoting the phosphorylation of extracellular signal‐regulated kinase 1/2, and disrupting the repair process of DNA double‐strand breaks. Moreover, fisetin serves as an adjunct therapy for the prevention and treatment of phosphatidylinositol‐4,5‐bisphosphate 3‐kinase catalytic subunit α (PIK3CA)‐mutant CRC, resulting in a reduction in phosphatidylinositol‐3 kinase (PI3K) expression, Ak strain transforming phosphorylation, mTOR activity, and downstream target proteins in CRC cells with a PIK3CA mutation. These findings highlight the multifaceted potential of fisetin in managing CRC and position it as a promising candidate for future therapy development.

show abstract

Future prospects in radiation oncology from the perspective of innovative radiation biology

Rödel,

Gaipl

2023

Strahlenther Onkol

View full text Add to dashboard Cite

YB-1 activating cascades as potential targets in KRAS-mutated tumors

Cited by 3 publications

References 236 publications

Emerging Therapies in Kirsten Rat Sarcoma Virus (+) Non-Small-Cell Lung Cancer

Emerging Therapies in Kirsten Rat Sarcoma Virus (+) Non-Small-Cell Lung Cancer

A comprehensive view on the fisetin impact on colorectal cancer in animal models: Focusing on cellular and molecular mechanisms

Future prospects in radiation oncology from the perspective of innovative radiation biology

Contact Info

Product

Resources

About