Anticancer effects of Lanostane against human gastric cancer cells involves autophagy, apoptosis and modulation of m-TOR/PI3K/AKT signalling pathway
Gastric carcinoma is the fourth leading cause of cancer-related morbidity throughout the globe. There are limited clinical therapies for gastric cancer due to lack of effective drugs and ambiguity in molecular mechanisms. As such there is a pressing need for novel and effective anticancer drugs for...
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Published in | Journal of B.U.ON. : official journal of the Balkan Union of Oncology Vol. 25; no. 3; p. 1463 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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Greece
01.05.2020
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Abstract | Gastric carcinoma is the fourth leading cause of cancer-related morbidity throughout the globe. There are limited clinical therapies for gastric cancer due to lack of effective drugs and ambiguity in molecular mechanisms. As such there is a pressing need for novel and effective anticancer drugs for gastric cancer. The main aim of the current research work was to investigate the anticancer effects of Lanostane natural product in MKN-45 human gastric cancer cells along with evaluating its effects on cell autophagy, apoptosis, and m-TOR/PI3K/AKT signalling pathway.
MTT cytotoxicity assay was used to evaluate cell viability of MKN-45 human gastric cancer cells. Apoptosis was evaluated by fluorescence microscopy using Hoechst 33258 and Annexin-V/propidium iodide (PI) assay using flow cytometry. Autophagy was evaluated by transmission electron microscopy (TEM) and western blot method. Effects on m-TOR/PI3K/AKT related protein expression were evaluated by western blot method.
Lanostane molecule led to substantial and dose-dependent growth inhibitory effects onMKN-45 human gastric cancer cells. Clonogenic assay showed significant decrease in MKN-45 cell colonies. Hoechst 33258 and annexin V/PI revealed that lanostane induced dominant apoptotic effects in these cells and exhibited dose-dependence. TEM revealed that lanostane induced autophagy in MKN-45 cells by forming autophagosomes and autophagic vacuoles. Lanostane also targeted m-TOR/PI3K/AKT signalling pathway by altering the expression of some key proteins.
Lanostane displayed strong anticancer effects in MKN-45 human gastric cancer cells by triggering apoptosis and autophagy and targeting m-TOR/PI3K/AKT signalling pathway. |
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AbstractList | Gastric carcinoma is the fourth leading cause of cancer-related morbidity throughout the globe. There are limited clinical therapies for gastric cancer due to lack of effective drugs and ambiguity in molecular mechanisms. As such there is a pressing need for novel and effective anticancer drugs for gastric cancer. The main aim of the current research work was to investigate the anticancer effects of Lanostane natural product in MKN-45 human gastric cancer cells along with evaluating its effects on cell autophagy, apoptosis, and m-TOR/PI3K/AKT signalling pathway.
MTT cytotoxicity assay was used to evaluate cell viability of MKN-45 human gastric cancer cells. Apoptosis was evaluated by fluorescence microscopy using Hoechst 33258 and Annexin-V/propidium iodide (PI) assay using flow cytometry. Autophagy was evaluated by transmission electron microscopy (TEM) and western blot method. Effects on m-TOR/PI3K/AKT related protein expression were evaluated by western blot method.
Lanostane molecule led to substantial and dose-dependent growth inhibitory effects onMKN-45 human gastric cancer cells. Clonogenic assay showed significant decrease in MKN-45 cell colonies. Hoechst 33258 and annexin V/PI revealed that lanostane induced dominant apoptotic effects in these cells and exhibited dose-dependence. TEM revealed that lanostane induced autophagy in MKN-45 cells by forming autophagosomes and autophagic vacuoles. Lanostane also targeted m-TOR/PI3K/AKT signalling pathway by altering the expression of some key proteins.
Lanostane displayed strong anticancer effects in MKN-45 human gastric cancer cells by triggering apoptosis and autophagy and targeting m-TOR/PI3K/AKT signalling pathway. |
Author | Luo, Renfeng Ruan, Changli Lei, Changjiang Cai, Yahong Lin, Jun He, Anbing Wang, Xia Dong, Weiguo Peng, Xiulan |
Author_xml | – sequence: 1 givenname: Xiulan surname: Peng fullname: Peng, Xiulan organization: Department of Oncology, the Fifth Hospital of Wuhan, Wuhan, Hubei Province, China, 430050 – sequence: 2 givenname: Changli surname: Ruan fullname: Ruan, Changli – sequence: 3 givenname: Changjiang surname: Lei fullname: Lei, Changjiang – sequence: 4 givenname: Anbing surname: He fullname: He, Anbing – sequence: 5 givenname: Xia surname: Wang fullname: Wang, Xia – sequence: 6 givenname: Renfeng surname: Luo fullname: Luo, Renfeng – sequence: 7 givenname: Yahong surname: Cai fullname: Cai, Yahong – sequence: 8 givenname: Weiguo surname: Dong fullname: Dong, Weiguo – sequence: 9 givenname: Jun surname: Lin fullname: Lin, Jun |
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SubjectTerms | Antineoplastic Agents - pharmacology Apoptosis - drug effects Autophagy - drug effects Cell Line, Tumor Cell Proliferation - drug effects Humans Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - drug effects Stomach Neoplasms - drug therapy Stomach Neoplasms - metabolism TOR Serine-Threonine Kinases - metabolism |
Title | Anticancer effects of Lanostane against human gastric cancer cells involves autophagy, apoptosis and modulation of m-TOR/PI3K/AKT signalling pathway |
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