PMID- 30590316
OWN - NLM
STAT- MEDLINE
DCOM- 20190613
LR  - 20190613
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 111
DP  - 2019 Mar
TI  - The preventive effect of deep sea water on the development of cancerous skin 
      cells through the induction of autophagic cell death in UVB-damaged HaCaT 
      keratinocyte.
PG  - 282-291
LID - S0753-3322(18)35586-0 [pii]
LID - 10.1016/j.biopha.2018.12.083 [doi]
AB  - Ultraviolet light (UV) is a major inducer of skin cancer. Therefore, recovery and 
      removal of UV-damaged skin cells are important in the prevention of skin 
      carcinogenesis. Here, we investigated the effect of deep sea water (DSW) in HaCaT 
      keratinocyte exposed by UVB (lambda = 290 approximately 320 nm). The result showed that UVB-induced 
      cell death was reinforced by DSW treatment in a hardness-dependent manner. 
      Furthermore, the increase of cell death by DSW was associated with the 
      down-regulation of survivin and RAD51 expressions induced by UVB. Moreover, we 
      confirmed the inhibition of H2 A.X phosphorylation, a marker for double-stranded 
      DNA damage, and the enhancement of LC3-II and SQSTM1/p62 expressions by DSW 
      administration in UVB-radiated HaCaT keratinocyte. The results imply that the 
      enhancement of UVB-induced cell death by DSW is associated with autophagy. 
      Therefore, we further explored the regulation of autophagy-regulating proteins 
      and apoptosis-related factors expression. Phosphorylation of mammalian target of 
      rapamycin (mTOR), ribosomal protein S6, and S6 kinase by UVB radiation were 
      regressed via DSW treatment, underlying the increase of AMP-activated protein 
      kinase (AMPK) phosphorylation. Furthermore, UVB-enhanced nuclear factor kappaB 
      (NF-kappaB) and c-Jun N-terminal kinase (JNK) phosphorylations were increased with 
      DSW treatment. Contrastingly, DSW lessened the Ser15 phosphorylation of p53 and 
      cleavage of poly (ADP-ribose) polymerase induced by UVB radiation. Consequently, 
      the results demonstrate that DSW enhances UVB-damaged skin cell clearance through 
      the activation of autophagic cell death underlying the regulation of 
      AMP-activated protein kinase (AMPK)/mTOR signaling as well as NF-kappaB and JNK 
      phosphorylations. In conclusion, this investigation suggests that DSW is a potent 
      candidate for the prevention of UV-induced skin cancer development.
CI  - Copyright (c) 2018 Elsevier Masson SAS. All rights reserved.
FAU - Lee, Kyu-Shik
AU  - Lee KS
AD  - Department of Pharmacology, School of Medicine and Intractable Disease Research 
      Center Dongguk University, Gyeongju, 38066, Republic of Korea.
FAU - Lee, Min-Gu
AU  - Lee MG
AD  - Department of Pharmacology, School of Medicine and Intractable Disease Research 
      Center Dongguk University, Gyeongju, 38066, Republic of Korea.
FAU - Woo, Yun-Jeong
AU  - Woo YJ
AD  - Department of Pharmacology, School of Medicine and Intractable Disease Research 
      Center Dongguk University, Gyeongju, 38066, Republic of Korea.
FAU - Nam, Kyung-Soo
AU  - Nam KS
AD  - Department of Pharmacology, School of Medicine and Intractable Disease Research 
      Center Dongguk University, Gyeongju, 38066, Republic of Korea. Electronic 
      address: namks@dongguk.ac.kr.
LA  - eng
PT  - Journal Article
DEP - 20181224
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
SB  - IM
MH  - Autophagy/physiology/*radiation effects
MH  - Carcinogenesis/pathology/*radiation effects
MH  - Cell Line
MH  - Cell Survival/physiology/radiation effects
MH  - Humans
MH  - Keratinocytes/pathology/*radiation effects
MH  - *Seawater
MH  - Skin Neoplasms/etiology/pathology/*prevention & control
MH  - Ultraviolet Rays/*adverse effects
OTO - NOTNLM
OT  - Autophagy
OT  - Deep sea water
OT  - HaCaT keratinocyte
OT  - Skin cancer
OT  - Ultraviolet B light
EDAT- 2018/12/28 06:00
MHDA- 2019/06/14 06:00
CRDT- 2018/12/28 06:00
PHST- 2018/08/10 00:00 [received]
PHST- 2018/12/17 00:00 [revised]
PHST- 2018/12/17 00:00 [accepted]
PHST- 2018/12/28 06:00 [pubmed]
PHST- 2019/06/14 06:00 [medline]
PHST- 2018/12/28 06:00 [entrez]
AID - S0753-3322(18)35586-0 [pii]
AID - 10.1016/j.biopha.2018.12.083 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2019 Mar;111:282-291. doi: 10.1016/j.biopha.2018.12.083. 
      Epub 2018 Dec 24.