Growth inhibitory effect and Chk1-dependent signaling involved in G2/M arrest on human gastric cancer cells induced by diallyl disulfide

Diallyl disulfide induces G2/M arrest and promotes apoptosis through the p53/p21 and MEK-ERK pathways in human esophageal squamous cell carcinoma

“…G2/M phase cell cycle arrest can reduce proliferation and induce apoptosis by inhibiting the segregation of damaged chromosomes during mitosis (15). DADS has been demonstrated to induce G2/M cell cycle arrest in several cancer cell lines such as colon cancer (11), breast cancer (12) and human gastric cancer cells (13). In the present study, we demonstrated that the percentage of ECA109 cells in DADS treatment groups significantly increased at the G2/M phase in a dosedependent manner (Fig.…”

“…DADS has a wide variety of biological activities including antifungal (5), antibacterial (6), antiviral (7), antioxidant (8), antiplatelet and antithrombotic properties (9). Moreover, DADS has gained increasing attention due to its protective effects of cancer development and anticancer effects against different types of malignancies (10)(11)(12)(13). Notably, the apoptotic effects of DADS were even superior to those of chemotherapy agents such as 5-Fu and CTX in human breast cancer cells (14).…”

Knock-down of human MutY homolog (hMYH) decreases phosphorylation of checkpoint kinase 1 (Chk1) induced by hydroxyurea and UV treatment

“…This means that hMYH is involved in the activation mechanism of Chk1 upon DNA damage, but not in stability or inactivation. Phospho-ATR (Ser428), which can be used to confirm the activation of ATR upon DNA damage and growth inhibition (16), was decreased in immunoprecipitates of siMYH-transfected cells treated with HU and UV irradiation. HU and UV-induced ATR phosphorylation were also dramatically diminished in hMYH-disrupted HaCaT cells (Fig.…”

Molecular characterization of the gene checkpoint homolog 1 in Daphnia carinata during different reproductive phases

“…Chk1 is the core molecular check for damaged DNA in G2/M. As a transducin, it can transmit amplifying signal to the effector Cdc25c, which enacts phosphorylation of Cdc25c to repair damaged DNA (Rouse and Jackson, 2002;Ling et al, 2010). Hence, when expression levels of Chk1 decrease, damaged DNA is no longer detected or repaired efficiently, which leads to cell apoptosis Syljuåsen et al, 2005;Bolderson et al, 2009;Carrassa et al, 2009).…”