BCL2L2 (BCL2 Like 2)

Since ABT-263 is unlikely to be approved for the clinical treatment of solid tumors due to both on-target (thrombocytopenia) and off-target (neutropenia) toxicities, the few studies indicating improved radiosensitivity with ABT-199 (venetoclax) are intriguing, suggesting that targeting of Bcl-xL may not be a strict requirement for the combination strategy. Finally, it is worth noting that senolytic agents have the potential to protect normal tissue from radiation-induced damage, which may prove to be the most clinically relevant observation for this class of drugs.

[This retracts the article DOI: 10.3727/096504016X14685034103879.].

The lead compounds, 44 and 46, demonstrated effective degradation of BCL-xL and, unexpectedly, degraded BCL-w, while sparing BCL-2. With further optimization, these BCL-xL and BCL-w dual-targeting PROTACs hold great promise as safer, more effective anticancer agents against BCL-xL and BCL-w codependent cancers.

In KATO III CSCs, DSBCl increased ID1 and MYC but decreased BCL2L1 and BAX. These findings suggest that DSBCl modulates critical markers and genes in gastric CSCs, highlighting its potential for gastric cancer treatment.

While Wsb2 is not essential in most cells, it is essential in cells derived from tumors of the nervous system, and knockdown of Wsb2 in these lines causes death by apoptosis. This work uncovers a novel mechanism of apoptosis regulation, with implications for developing therapies against neuroblastomas and other cancers reliant on this pathway for survival.

Accumulating evidence positions PUMA as a universal sensor of cell death stimuli and a promising therapeutic target in cancer. This article critically examines PUMA's regulation, function, and potential as a target for cancer treatment.

Pharmacological inhibition using BH3 mimetic compounds against MCL-1, but not BCL-2, BCL-XL, or BCL-w, killed HTLV-1c-infected cells in vitro and in vivo and significantly delayed disease progression when combined with tenofovir and dolutegravir in mice. Our data suggest that combination antiretroviral therapy with MCL-1 antagonism may represent an effective, clinically relevant, and potentially curative strategy against HTLV-1c.

The results highlighted genes with possible roles in apoptosis and acting in breast carcinogenesis. In particular, BIRC5 was shown as important oncogene and ZEB1 as a tumor suppressor in invasive breast cancer. Further studies are warranted to evaluate the potential of the investigated genes as biomarkers or therapeutic targets, with possible implications for breast cancer diagnosis and treatment.

Based on these results, butylcycloheptyl prodigiosin and prodigiosin-R2 could be more effective BH3 mimetics and should be further studied.

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.

This study is the first to demonstrate that compound 5 inhibits the growth of U87 glioma cells in vitro and in vivo through a biphasic dose-dependent switch from cell cycle arrest to apoptosis in a p21 level-dependent manner. These findings suggest that naphthalimide-based compounds can serve as lead compounds for designing new and more potent anti-glioma drugs.

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