-“CHOP-dependent death receptor 5 induction is a major component...” by Yidan Lin et al. has been accepted for publication in Cancer Research.

-“The natural product honokiol preferentially inhibits c-FLIP...” by Shruti M. Raja et al. has been accepted for publication in Molecular Cancer Therapeutics.

-“PPARg and apoptosis in cancer” by Heath Elrod and Shi-Yong Sun has been accepted for publication in PPAR Research.

-Congratulations to Dr. Xiangguo Liu, who has been offered the position of Professor from Shandong University, P. R. China. He will leave in August.

The Lung Cancer Research Laboratory Members

Targeted cancer therapies represent a major advance in our fight against cancer. However, it has been increasingly recognized that dysregulated survival mechanisms not only contribute to tumorigenesis, but also induce resistance to therapies, thus decreasing their treatment efficacy. The long-term goal of our research is to develop novel and efficacious therapeutic regimens for the treatment of human cancer based on our mechanistic studies on cancer biology.

Apoptosis represents one of the main types of cell suicide mechanism. Inducing apoptosis has been implicated as the primary strategy to treat cancers such as chemotherapy or radiotherapy. It is well known that apoptosis occurs through two main cellular pathways: the intrinsic mitochondrial pathway involving cytochrome C release, apoptosome formation and subsequent caspase-9 activation and the extrinsic death receptor pathway relying on trimerization of cell surface death receptors and activation of caspase-8. Through caspase-8-mediated truncation of Bid, the extrinsic apoptotic pathway can also activate the intrinsic apoptotic pathway (Fig. 1). The major research interest in our lab is to study the mechanism(s) underlying regulation of the expression of death receptors and their implications in drug-induced apoptosis.

PI3K/AKT/mTOR signaling is hyper-activated in many types of cancers including lung cancer; so intervention of mTOR pathway can serves as an attractive cancer therapeutic target. The rapamycin derivatives, RAD001 and CCI-779, are currently tested in various clinical trials. In addition to regulation of mTOR (mTORC1) by Akt, recent studies have reveled that mTOR (mTORC2) can also activates Akt, thus locating mTOR on both upstream and downstream of Akt (Fig. 2). A newly developed research area in our lab is to study the relationship between mTOR and Akt signaling pathways and the impact of mTOR-inhibition-mediated Akt activation on mTOR-targeted cancer therapy. We are particularly interested in the mechanisms underlying mTOR inhibition-induced Akt activation.