Live-cell FRET assay on the stoichiometry and affinity of the YAP complexes in MCF-7 cells.

Yes-associated protein (YAP), a focal point of current biological research, is involved in regulating various life processes. In this report, live-cell fluorescence resonance energy transfer (FRET) imaging was employed to unravel the YAP complexes in MCF-7 cells. Fluorescence imaging of living cells co-expressing CFP (cyan fluorescent protein)-YAP and YFP (yellow fluorescent protein)-LATS1 (large tumor suppressor 1) plasmids revealed that YAP promoted LATS1 oligomerization around mitochondria.

YAP upregulates AMPKα1 to induce cancer cell senescence.

Yes-associated protein (YAP)-a major effector protein of the Hippo pathway- regulates cell proliferation, differentiation, apoptosis, and senescence. Amp-activated protein kinase (AMPK) is a key sensor that monitors cellular nutrient supply and energy status. Although YAP and AMPK are considered to regulate cellular senescence, it is still unclear whether AMPK is involved in YAP-regulated cellular senescence.

Sirt3 activates autophagy to prevent DOX-induced senescence by inactivating PI3K/AKT/mTOR pathway in A549 cells.

Sirtuin 3 (Sirt3), a mitochondrial deacetylase, regulates mitochondrial redox homeostasis and autophagy and is involved in physiological and pathological processes such as aging, cellular metabolism, and tumorigenesis. We here investigate how Sirt3 regulates doxorubicin (DOX)-induced senescence in lung cancer A549 cells. Sirt3 greatly reduced DOX-induced upregulation of senescence marker proteins p53, p16, p21 and SA-β-Gal activity as well as ROS levels.

BID- and BAX-mediated mitochondrial pathway dominates A-1331852-induced apoptosis in senescent A549 cells.

Recovered senescent tumor cells harbor higher migration and invasion potential, owing to which they play a crucial role in tumor recurrence and drug resistance. The aim of this study was to explore the ability of BH3 mimetics in clearing senescent A549 cells and elucidate their underlying killing mechanism. Doxorubicin-induced cell senescence was determined using augmented senescence-associated beta-galactosidase (SA-β-Gal) staining and increased P16 expression.

BAK plays a key role in A-1331852-induced apoptosis in senescent chondrocytes.

Osteoarthritis occurs when the number of senescent chondrocytes in the joints reaches an intolerable level. The purpose of our study was to explore the therapeutic effect and mechanism of action of A-1331852 in osteoarthritis. Doxorubicin and etoposide were used to induce cell senescence as determined by the cessation of cell proliferation, augmented senescence-associated beta-galactosidase (SA-β-Gal) staining, and increased p53 expression levels.

Bim- and Bax-mediated mitochondrial pathway dominates abivertinib-induced apoptosis and ferroptosis.

Abivertinib (AC) is a novel epidermal growth factor receptor tyrosine kinase inhibitor with highly efficient antitumor activity. Here, we report the capacity of AC to induce both reactive oxygen species (ROS)-dependent apoptosis and ferroptosis in tumor cells. Our data showed that AC induced iron- and ROS-dependent cytotoxicity in MCF7, HeLa, and A549 cell lines.

Bak instead of Bax plays a key role in metformin-induced apoptosis s in HCT116 cells.

Metformin (Met) exhibits anticancer ability in various cancer cell lines. This report aims to explore the exact molecular mechanism of Met-induced apoptosis in HCT116 cells, a human colorectal cancer cell line. Met-induced reactive oxygen species (ROS) increase and ROS-dependent cell death accompanied by plasma membrane blistering, mitochondrial swelling, loss of mitochondrial membrane potential, and release of cytochrome c.

Reduction of SIRT1 Mediates Monosodium Iodoacetate-Induced Osteoarthritic Pain by Upregulating p53 Expression in Rats.

Background: Clinically, chronic pain is the most common and disabling symptom of osteoarthritis (OA). OA pain is associated with OA lesion of the knee and the plastic changes in the peripheral and central nervous systems. However, the central mechanisms involved at the spinal cord level are not fully understood.