PMID- 31786875
OWN - NLM
STAT- MEDLINE
DCOM- 20200428
LR  - 20211204
IS  - 2241-6293 (Electronic)
IS  - 1107-0625 (Linking)
VI  - 24
IP  - 5
DP  - 2019 Sep-Oct
TI  - Targeted antitumor activity of Ginsenoside (Rg1) in paclitaxel-resistant human 
      nasopharyngeal cancer cells are mediated through activation of autophagic cell 
      death, cell apoptosis, endogenous ROS production, S phase cell cycle arrest and 
      inhibition of m-TOR/PI3K/AKT signalling pathway.
PG  - 2056-2061
AB  - PURPOSE: Nasopharyngeal carcinoma is one of common and vicious cancers of head 
      and neck. The main purpose of this study was to examine the anticancer effects of 
      the naturally occurring compound Ginsenoside (Rg1) against paclitaxel-resistant 
      human nasopharyngeal cancer cells along with evaluation of its effects on cell 
      autophagy, apoptosis, ROS production, cell cycle progression and m-TOR/PI3K/AKT 
      signalling pathway. METHODS: The viability of SUNE1 cancer cell line and NP460 
      normal cell line was checked by CCK8 counting assay. Apoptosis-related studies 
      were examined by fluorescent microscopy using acridine orange (AO)/ethidium 
      bromide (EB) staining as well as flow cytometry using annexin V assay. Further, 
      transmission electron microscopy (TEM) was used to study autophagic effects 
      induced by Ginsenoside (Rg1). Western blot assay was used to study the effects of 
      Ginsenoside on apoptosis and on autophagy-related protein expressions including 
      Bax, Bcl-2, LC3-ll. RESULTS: The results indicated that Ginsenoside (Rg1) reduces 
      the viability of the nasopharyngeal carcinoma cells in a dose-dependent manner, 
      showing IC50 of 15 microM in cancer cells and IC50 of 80 microM in normal cell lines. The 
      AO/EB staining showed that Ginsenoside (Rg1) inhibits the viability of cancer 
      cells via induction of apoptotic cell death which was correlated with increase in 
      Bax and decrease in Bcl-2 levels. Electron microscopic analysis showed that 
      Ginsenoside (Rg1) caused the development of autophagosomes in cancer cells. 
      Similarly, Ginsenoside (Rg1) increased the expression of LC3-II protein, 
      indicating autophagic cell death. Ginsenoside (Rg1) also induced dose-dependent S 
      phase cell cycle arrest. Western blot analysis showed that Ginsenoside (Rg1) has 
      the potential to block m-TOR/PI3K/AKT signalling pathway. CONCLUSIONS: In 
      conclusion, the results of this study clearly indicate that Ginsenoside (Rg1) 
      could be developed as a potent candidate drug against nasopharyngeal cancer 
      provided further in vivo studies as well as toxicological studies are carried 
      out.
FAU - Li, Wei
AU  - Li W
AD  - Department of Otolaryngology, Ezhou Central Hospital, Ezhou City, Hubei Province, 
      P.R. China, 436000.
FAU - Li, Guangyi
AU  - Li G
FAU - She, Wensheng
AU  - She W
FAU - Hu, Xian
AU  - Hu X
FAU - Wu, Xingyu
AU  - Wu X
LA  - eng
PT  - Journal Article
PL  - Cyprus
TA  - J BUON
JT  - Journal of B.U.ON. : official journal of the Balkan Union of Oncology
JID - 100883428
RN  - 0 (BCL2 protein, human)
RN  - 0 (Ginsenosides)
RN  - 0 (MAP1LC3B protein, human)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Oncogene Protein v-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - P88XT4IS4D (Paclitaxel)
RN  - PJ788634QY (ginsenoside Rg1)
SB  - IM
MH  - Apoptosis/drug effects
MH  - Autophagy/*drug effects
MH  - Cell Cycle Checkpoints/drug effects
MH  - Cell Line, Tumor
MH  - Drug Resistance, Neoplasm/*drug effects
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Ginsenosides/*pharmacology
MH  - Humans
MH  - Microtubule-Associated Proteins/genetics
MH  - Nasopharyngeal Neoplasms/*drug therapy/genetics/pathology
MH  - Oncogene Protein v-akt/genetics
MH  - Paclitaxel/adverse effects/pharmacology
MH  - Phosphatidylinositol 3-Kinases/genetics
MH  - Proto-Oncogene Proteins c-bcl-2/genetics
MH  - Reactive Oxygen Species/metabolism
MH  - S Phase Cell Cycle Checkpoints/drug effects
MH  - Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/genetics
EDAT- 2019/12/02 06:00
MHDA- 2020/04/29 06:00
CRDT- 2019/12/02 06:00
PHST- 2019/12/02 06:00 [entrez]
PHST- 2019/12/02 06:00 [pubmed]
PHST- 2020/04/29 06:00 [medline]
PST - ppublish
SO  - J BUON. 2019 Sep-Oct;24(5):2056-2061.