oblongifolin-c and Colonic-Neoplasms

oblongifolin-c has been researched along with Colonic-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for oblongifolin-c and Colonic-Neoplasms

Article	Year
DNA damage and ER stress contribute to oblongifolin C-induced cell killing in Bax/Bak-deficient cells. Biochemical and biophysical research communications, 2015, Feb-13, Volume: 457, Issue:3 A key clinical problem in oncology is the treatment of apoptosis-resistant tumors. Tumor cells deficient in both of the proapoptotic proteins Bax and Bak are protected against most chemotherapeutic drug-induced apoptosis. We report here that a natural compound, oblongifolin C (OC), effectively eliminates Bax/Bak-deficient murine embryonic fibroblasts and colon carcinoma HCT116 cells. OC not only triggers DNA double-strand breaks and DNA damage response, but also inhibits repair of DNA damage. In addition, OC induces ER stress through upregulation of the transcription factor CHOP and activation of JNK kinases. Upon treatment with OC, cells undergo Bax/Bak-independent, caspase-mediated apoptosis. Taken together, our data establish a rationale for the broad use of OC to treat apoptosis deficient tumors. Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; bcl-2 Homologous Antagonist-Killer Protein; bcl-2-Associated X Protein; Caspases; Cells, Cultured; Colonic Neoplasms; DNA Breaks, Double-Stranded; DNA Damage; DNA Repair; Endoplasmic Reticulum Stress; HCT116 Cells; Humans; Mice; Mice, Knockout; Terpenes	2015

Article

Year

DNA damage and ER stress contribute to oblongifolin C-induced cell killing in Bax/Bak-deficient cells.

Biochemical and biophysical research communications, 2015, Feb-13, Volume: 457, Issue:3

A key clinical problem in oncology is the treatment of apoptosis-resistant tumors. Tumor cells deficient in both of the proapoptotic proteins Bax and Bak are protected against most chemotherapeutic drug-induced apoptosis. We report here that a natural compound, oblongifolin C (OC), effectively eliminates Bax/Bak-deficient murine embryonic fibroblasts and colon carcinoma HCT116 cells. OC not only triggers DNA double-strand breaks and DNA damage response, but also inhibits repair of DNA damage. In addition, OC induces ER stress through upregulation of the transcription factor CHOP and activation of JNK kinases. Upon treatment with OC, cells undergo Bax/Bak-independent, caspase-mediated apoptosis. Taken together, our data establish a rationale for the broad use of OC to treat apoptosis deficient tumors.

Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; bcl-2 Homologous Antagonist-Killer Protein; bcl-2-Associated X Protein; Caspases; Cells, Cultured; Colonic Neoplasms; DNA Breaks, Double-Stranded; DNA Damage; DNA Repair; Endoplasmic Reticulum Stress; HCT116 Cells; Humans; Mice; Mice, Knockout; Terpenes

2015