Correction: LACTB exerts tumor suppressor properties in epithelial ovarian cancer through regulation of Slug.

We show the ability of LACTB to function as a tumor suppressor in ovarian cancer through down-regulation of Slug and induction of differentiation.

LACTB induces cancer cell death through the activation of the intrinsic caspase-independent pathway in breast cancer.

Background: LACTB was recently identified as a mitochondrial tumour suppressor that negatively affects cancer cell proliferation by inducing cell death and/or differentiation, depending on the cell type and tissue. However, the detailed mechanism underlying the LACTB-induced cancer cell death is largely unknown.

Methods: We used cell-based, either in 2D or 3D conditions, and in vivo experiments to understand the LACTB mechanisms.

Analysis of 5-Azacytidine Resistance Models Reveals a Set of Targetable Pathways.

The mechanisms by which myelodysplastic syndrome (MDS) cells resist the effects of hypomethylating agents (HMA) are currently the subject of intensive research. A better understanding of mechanisms by which the MDS cell becomes to tolerate HMA and progresses to acute myeloid leukemia (AML) requires the development of new cellular models. From MDS/AML cell lines we developed a model of 5-azacytidine (AZA) resistance whose stability was validated by a transplantation approach into immunocompromised mice.

SMAD4 loss limits the vulnerability of pancreatic cancer cells to complex I inhibition via promotion of mitophagy.

Pancreatic cancer is one of the deadliest forms of cancer, which is attributed to lack of effective treatment options and drug resistance. Mitochondrial inhibitors have emerged as a promising class of anticancer drugs, and several inhibitors of the electron transport chain (ETC) are being clinically evaluated. We hypothesized that resistance to ETC inhibitors from the biguanide class could be induced by inactivation of SMAD4, an important tumor suppressor involved in transforming growth factor β (TGFβ) signaling, and associated with altered mitochondrial activity.