PMID- 29731854
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1792-1074 (Print)
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Linking)
VI  - 15
IP  - 5
DP  - 2018 May
TI  - Cantharidin suppresses cell growth and migration, and activates autophagy in 
      human non-small cell lung cancer cells.
PG  - 6527-6532
LID - 10.3892/ol.2018.8141 [doi]
AB  - Cantharidin (CTD), a component of Mylabris (blister beetle), is a traditional 
      Chinese medicine that exerts an anticancer effect in multiple types of cancer 
      cells. The aim of the present study was to investigate whether CTD exhibited 
      anti-metastatic and inhibitory cell proliferation effects against human non-small 
      cell lung cancer (NSCLC) A549 cells, and the possible underlying mechanism by 
      which this occurs. The results of the present study demonstrated that CTD 
      arrested proliferation, suppressed invasion and migration and induced apoptosis 
      in A549 cells in vitro. Alterations of apoptosis-associated protein levels, 
      including B-cell lymphoma-2 (Bcl-2), Bcl-associated X (Bax) and active caspase-3, 
      were detected. Furthermore, the present study demonstrated that CTD activated 
      autophagy through downregulation of p62 expression and upregulation of 
      microtubule-associated proteins 1A/1B light chain 3B and Beclin-1 expression. 
      Additionally, western blot analysis identified that CTD inhibited the 
      phosphatidylinositol 3-kinase (PI3K)/RAC serine/threonine protein kinase 
      (Akt)/mechanistic target of rapamycin (mTOR) signaling pathway in NSCLC, 
      demonstrating that the levels of phosphorylated (p-)Akt, p-mTOR, phosphorylated 
      ribosomal p70S6 protein kinase (p-p70-S6K) and cyclin D1 were significantly 
      decreased following treatment with CTD. In conclusion, the results of the present 
      study indicated that CTD impeded cell growth and migration by inhibiting 
      PI3K/Akt/mTOR signaling in NSCLC, and promoted autophagy and apoptosis. CTD 
      exhibited anticancer activity against NSCLC in vitro, revealing it as a potential 
      candidate for the treatment of NSCLC.
FAU - Liu, Yan-Peng
AU  - Liu YP
AD  - Department of Internal Medicine, The Second Hospital of Shandong University, 
      Jinan, Shandong 250033, P.R. China.
FAU - Li, Ling
AU  - Li L
AD  - Department of Surgery, Affiliated Hospital of Shandong Academy of Medical 
      Sciences, Jinan, Shandong 250031, P.R. China.
FAU - Xu, Liang
AU  - Xu L
AD  - Department of Surgery, Affiliated Hospital of Shandong Academy of Medical 
      Sciences, Jinan, Shandong 250031, P.R. China.
FAU - Dai, E-Nuo
AU  - Dai EN
AD  - Department of Surgery, Affiliated Hospital of Shandong Academy of Medical 
      Sciences, Jinan, Shandong 250031, P.R. China.
FAU - Chen, Wei-Da
AU  - Chen WD
AD  - Department of Geriatric Medicine, Affiliated Hospital of Shandong University of 
      Traditional Chinese Medicine, Jinan, Shandong 250014, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20180301
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC5920915
OTO - NOTNLM
OT  - autophagy
OT  - cantharidin
OT  - non-small cell lung cancer cell
OT  - phosphoinositide 3-kinase/RAC serine/threonine-protein kinase/mechanistic target 
      of rapamycin signaling pathway
OT  - proliferation
EDAT- 2018/05/08 06:00
MHDA- 2018/05/08 06:01
PMCR- 2018/03/01
CRDT- 2018/05/08 06:00
PHST- 2017/06/16 00:00 [received]
PHST- 2017/12/05 00:00 [accepted]
PHST- 2018/05/08 06:00 [entrez]
PHST- 2018/05/08 06:00 [pubmed]
PHST- 2018/05/08 06:01 [medline]
PHST- 2018/03/01 00:00 [pmc-release]
AID - OL-0-0-8141 [pii]
AID - 10.3892/ol.2018.8141 [doi]
PST - ppublish
SO  - Oncol Lett. 2018 May;15(5):6527-6532. doi: 10.3892/ol.2018.8141. Epub 2018 Mar 1.