Abstract: Blocking peptides that inhibit FAK or NANOG binding to Cx26, and a method of treating cancer by administering these blocking peptides to a subject in need thereof are described.

Abstract: Provided herein are compositions, systems, kits, and methods for treating cancer by administering to a subject an agent that inhibits a target mRNA or target protein selected from ROR2, JNK1, LCK, LIME, BRCA1, and MLH1. In certain embodiments, the cancer is a uterine or ovarian cancer. In some embodiments, the cancer is chemotherapy refractory cancer (e.g., Cisplatin resistant cancer). In particular embodiments, the subject is further administered an anti-cancer agent (e.g., the agent sensitizes the cancer cells to treatment with an anti-cancer agent, such as Cisplatin).

Abstract: Blocking peptides that inhibit FAK or NANOG binding to Cx26, and a method of treating cancer by administering these blocking peptides to a subject in need thereof are described.

Abstract: It has now been demonstrated that syndecan binds to and interacts with MC4-R, and thereby modulates neuropeptide regulation of body weight, via the agouti/MC4-R signaling pathway. Transgenic animals were made initially using a construct including a cytomegalovirus promoter and the 3′ untranslated region, including the polyadenylation site, of the bovine growth hormone gene, as well as cDNA encoding syndecan-1. The mice express the syndecan-1 transgene in many tissues, with expression in the brain occurring preferentially in their hypothalamus. These mice are characterized by elevated levels of circulating syndecan-1 ectodomain and exhibit enormous weight gain after reaching sexual maturity, but have a relatively normal distribution of fat, are completely healthy and heterozygotes reproduce, and show other indicators associated with obesity in humans. Agouti mice which are transgenic for syndecan-1 ectodomain demonstrate that syndecan-1 and agouti interact, potentiating obesity.