We are analyzing https://link.springer.com/article/10.1186/s12935-019-1054-0.

Title:
Blocking AMPK/ULK1-dependent autophagy promoted apoptosis and suppressed colon cancer growth | Cancer Cell International
Description:
Background Autophagy is an evolutionarily conserved process through which cells degrade and recycle cytoplasm. The relation among autophagy, apoptosis and tumor is highly controversial until now and the molecular mechanism is poorly understood. Methods Cell viability and apoptosis were detected by CCK8, crystal violet staining, Hoechst333342 staining and flow cytometry. The expression of AMPK and ULK1 was analyzed by western blotting. Colon cancer growth suppression by NVP-BEZ235 or CQ in vivo was studied in a tumor xenograft mouse model. Results Our previous study revealed that NVP-BEZ235 suppressed colorectal cancer growth via inducing apoptosis, however later, we found it also initiated autophagy simultaneously. In this present study, our results show that NVP-BEZ235 induced autophagy through AMPK/ULK1 pathway in colon cancer cells. Blocking autophagy by knocking down AMPK or ULK1 inhibited cell proliferation and further promoted NVP-BEZ235 induced apoptosis. Meantime, the autophagy inhibitor chloroquine (CQ) shows obvious effect on inhibiting cell proliferation but not on inducing apoptosis, while it significantly increased NVP-BEZ235 induced apoptosis. Furthermore, the combinational therapy of NVP-BEZ235 and CQ shows synergistic antitumor effects in colon cancer in vivo. Conclusion NVP-BEZ235 induced AMPK/ULK1-dependent autophagy. Targeting this autophagy suppressed colon cancer growth through further promoting apoptosis, which is a potential therapeutic option for clinical patients.
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Keywords {🔍}

nvpbez, autophagy, cancer, apoptosis, cell, cells, colon, article, treatment, fig, google, scholar, ampk, hct, ulk, cas, tumor, combinational, results, lcii, growth, zhang, expression, induced, therapy, rko, shown, colorectal, ampkulk, wang, study, pathway, vivo, detected, inhibitor, antitumor, therapeutic, human, mtor, treated, tumors, analysis, liu, viability, staining, western, blotting, effects, gfplc, mice,

Topics {✒️}

targeting pi3k/akt/mtor signaling anti-cancer drugs nvp-bez235 pi3k/akt/mtor pathway inhibitors dual pi3k/mtor inhibitor 4ebp1/eif4e/puma pathway anti-mouse secondary antibody pi3k/akt/mtor signalling full size image anti-mouse secondary antibodies amp-activated protein kinase nvp-bez235-induced apoptosis p53-ros cross-talk nvp-bez235 induced autophagy mccoy’s5a modified media ampk/ulk1 promoted apoptosis nvp-bez235 induces autophagy hrp-conjugated anti-rabbit article download pdf significant anti-tumor effect phosphate-buffered saline solution 500 ml dmem/mccoy’s5a ice-cold lysis buffer fluorescence-activated cell sorting mitochondrial–lysosomal cross-talk ampk/ulk1 dependent nvp-bez235 induce autophagy xenograft mouse model 40 mg/kg nvp-bez235 suppress tumor growth ampk/ulk1 axis firstly nat cell biol conjugated anti-rabbit related subjects synergistic antitumor activity including colon cancer treating human tumors basic research program full access colon cancer cells privacy choices/manage cookies autophagy related gene anti-tumor drugs nvp-bez235 increased cell apoptosis increased fundamental research funds nvp-bez235 upregulation mol cancer ther colon cancer therapy pi3k/mtor pathways negatively regulates autophagy

Questions {❓}

The crosstalk between autophagy and apoptosis: where does this lead?

Schema {🗺️}

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         description:Autophagy is an evolutionarily conserved process through which cells degrade and recycle cytoplasm. The relation among autophagy, apoptosis and tumor is highly controversial until now and the molecular mechanism is poorly understood. Cell viability and apoptosis were detected by CCK8, crystal violet staining, Hoechst333342 staining and flow cytometry. The expression of AMPK and ULK1 was analyzed by western blotting. Colon cancer growth suppression by NVP-BEZ235 or CQ in vivo was studied in a tumor xenograft mouse model. Our previous study revealed that NVP-BEZ235 suppressed colorectal cancer growth via inducing apoptosis, however later, we found it also initiated autophagy simultaneously. In this present study, our results show that NVP-BEZ235 induced autophagy through AMPK/ULK1 pathway in colon cancer cells. Blocking autophagy by knocking down AMPK or ULK1 inhibited cell proliferation and further promoted NVP-BEZ235 induced apoptosis. Meantime, the autophagy inhibitor chloroquine (CQ) shows obvious effect on inhibiting cell proliferation but not on inducing apoptosis, while it significantly increased NVP-BEZ235 induced apoptosis. Furthermore, the combinational therapy of NVP-BEZ235 and CQ shows synergistic antitumor effects in colon cancer in vivo. NVP-BEZ235 induced AMPK/ULK1-dependent autophagy. Targeting this autophagy suppressed colon cancer growth through further promoting apoptosis, which is a potential therapeutic option for clinical patients.
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      headline:Blocking AMPK/ULK1-dependent autophagy promoted apoptosis and suppressed colon cancer growth
      description:Autophagy is an evolutionarily conserved process through which cells degrade and recycle cytoplasm. The relation among autophagy, apoptosis and tumor is highly controversial until now and the molecular mechanism is poorly understood. Cell viability and apoptosis were detected by CCK8, crystal violet staining, Hoechst333342 staining and flow cytometry. The expression of AMPK and ULK1 was analyzed by western blotting. Colon cancer growth suppression by NVP-BEZ235 or CQ in vivo was studied in a tumor xenograft mouse model. Our previous study revealed that NVP-BEZ235 suppressed colorectal cancer growth via inducing apoptosis, however later, we found it also initiated autophagy simultaneously. In this present study, our results show that NVP-BEZ235 induced autophagy through AMPK/ULK1 pathway in colon cancer cells. Blocking autophagy by knocking down AMPK or ULK1 inhibited cell proliferation and further promoted NVP-BEZ235 induced apoptosis. Meantime, the autophagy inhibitor chloroquine (CQ) shows obvious effect on inhibiting cell proliferation but not on inducing apoptosis, while it significantly increased NVP-BEZ235 induced apoptosis. Furthermore, the combinational therapy of NVP-BEZ235 and CQ shows synergistic antitumor effects in colon cancer in vivo. NVP-BEZ235 induced AMPK/ULK1-dependent autophagy. Targeting this autophagy suppressed colon cancer growth through further promoting apoptosis, which is a potential therapeutic option for clinical patients.
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