CDK2 expression

The cytotoxic effect of engineered T-cells was tested against Rituximab-resistant DLBCL cells (RR-NU-DUL-1)...These findings suggest that CAR T-cell therapy holds great promise for treating refractory DLBCL, offering a potential path for clinical application. This in vitro evaluation highlights the potential of WEE1-engineered T-cells as a targeted treatment strategy for refractory DLBCL, emphasizing their clinical applicability and ability to overcome resistance mechanisms in this aggressive lymphoma subtype.

Combination of CDK2 inhibitors in clinical trials (Dinaciclib or PF-07104091) and lenvatinib markedly suppressed growth of xenograft tumors from the lenvatinib-resistant patient. The findings support the combination therapy strategy of lenvatinib and CDK2 inhibitor for lenvatinib-resistant ATC patients with high CDK2 expression.

It is typically responsive to anthracycline/taxol-based conventional chemotherapy...These data identify potential mechanistic leads for anti-proliferative and pro-apoptotic effects of DF in the present TNBC model. The present experiments validated a mechanism-driven experimental approach to identify efficacious nutritional herbs and/or their bioactive constituents as treatment alternatives for TNBC.

Further, in-silico studies identified Losartan and Allopurinol, with docking scores of -7.11 and -6.219, respectively, as potential repurposable drugs. The treatment of HepG2 cells with Allopurinol resulted in significant downregulation of CCNA2/CDK2 expression with an elevation in reactive oxygen species levels, uncovering Allopurinol's anticancer mechanism through cellular apoptosis. This study suggests the importance of RWD in drug repurposing and the potential of Allopurinol as a repurposable drug against HCC.

CDK4/6 inhibitors such as palbociclib block cell cycle progression and improve outcomes for many ER+/HER2- breast cancer patients...Understanding the molecular mechanisms that allow treated tumor cells to evade arrest is critical for identifying targets of future therapies. Ultimately, we seek to further SPCA as a tool of precision medicine, targeting treatments by individual tumors, and extending this computational framework to interpret other cyclical biological processes represented by high-dimensional data.

This effect was associated with upregulation of the CDK inhibitor p21 and downregulation of cyclin D1, cyclin E, CDK4, and CDK2 expression. Our data indicated that CAE exerted anti-proliferative activity by activating the mitochondria-mediated caspase-dependent apoptotic pathway and arresting the p21-mediated G0/G1 cell cycle on human gastric cancer AGS cells.

The expression of messenger RNA for cyclin A1, cyclin-dependent kinase 2 (CDK2), matrix metallopeptidase 2 (MMP2), and bcl-2 associated x protein (Bax) is regulated by PDPK1 under estrogen treatment. Our results indicated that PDPK1 plays a role as an oncogene in the development of EOC; hence, elucidating the mechanism by which estrogen promotes EOC progression by regulating PDPK1 expression.

This lays a solid foundation for further exploring the pharmacological role of SANG in CA therapy. However, further in-depth in vitro and in vivo experiments are required to corroborate our findings.

Gene expression analysis showed the downregulation of CDK2 and upregulation of the BAX/BCL2 ratio. Atomistic insight was studied on HPV 16 E6 via molecular dynamics simulation, revealing key interactions between tyrosinyl portion and C51 residue.

Collectively, these findings suggest that CARD16 is a tumor-promoting molecular in glioma via downregulating FOXO1/TRAIL axis, and suppressing TRAIL-induced apoptosis. The CARD16 gene presents significant potential for prognostic prediction and advances in innovative apoptotic therapeutics.

Furthermore, western blot analysis revealed that Biochanin A-treated cells exhibited lower expression of the Bcl-2, p-PI3K and p-AKT and higher expression of proapoptotic genes, including Bax, Caspase-3, Caspase-9, and cytochrome c. Additionally, PCR array analysis indicated that the gene expression levels of cyclin D3, cyclin B1, CDK1, CDK2, and CDK4 were downregulated, while the expression levels of p21, p27, and p53 were significantly upregulated. These results suggest that Biochanin A can suppress the viability of breast cancer cells and induce apoptosis via the mitochondrial pathway, along with inhibition of the Pi3K/Akt signaling pathway and modulation of cell cycle markers.

4i also demonstrated a high potential for oral bioavailability due to its adherence to Lipinski's rule of five. The molecular docking studies of 4i analog showed good binding mode with CDK6 active pocket through the formation of multiple interactions with its key amino acids.