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Methylsulfonylmethane Induces G1 Arrest and Mitochondrial Apoptosis in YD-38 Gingival Cancer Cells.

Abstract Gingival squamous cell carcinoma is a rare form of cancer that accounts for less than 10% of all head and neck cancers. Targeted therapies with natural compounds are of interest because they possess high efficacy with fewer side-effects. Methylsulfonylmethane (MSM) is an organic sulfur-containing compound with anticancer activities. The main goal of this study was to induce proliferation inhibition and apoptosis in the metastatic YD-38 cell line. MSM up-regulated expression of P21(Waf1/Cip1) and P27(Kip1) genes and down-regulated expression of cyclin D1 (CCND1) and CDK4. Moreover, treatment with MSM induced apoptosis and up-regulation of BAX in YD-38 cells. In accordance, the expression of the BCL-2 and BCL-XL, were inhibited, indicating the role of mitochondria in MSM-induced apoptosis. Analysis of mitochondrial integrity showed a loss of mitochondrial potential with an increased level of cytochrome c in the cytosol compared to mitochondria. Active CASPASE-3 (CASP3) was also observed, confirming that MSM-induced apoptosis is caspase-mediated.
PMID
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Authors

Mayor MeshTerms
Keywords

BAX-BCL-2

CYC

G1 arrest

MSM

mitochondrial apoptosis

Journal Title anticancer research
Publication Year Start




PMID- 28373424
OWN - NLM
STAT- MEDLINE
DA  - 20170404
DCOM- 20170413
LR  - 20170413
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 37
IP  - 4
DP  - 2017 Apr
TI  - Methylsulfonylmethane Induces G1 Arrest and Mitochondrial Apoptosis in YD-38
      Gingival Cancer Cells.
PG  - 1637-1646
AB  - Gingival squamous cell carcinoma is a rare form of cancer that accounts for less 
      than 10% of all head and neck cancers. Targeted therapies with natural compounds 
      are of interest because they possess high efficacy with fewer side-effects.
      Methylsulfonylmethane (MSM) is an organic sulfur-containing compound with
      anticancer activities. The main goal of this study was to induce proliferation
      inhibition and apoptosis in the metastatic YD-38 cell line. MSM up-regulated
      expression of P21Waf1/Cip1 and P27Kip1 genes and down-regulated expression of
      cyclin D1 (CCND1) and CDK4. Moreover, treatment with MSM induced apoptosis and
      up-regulation of BAX in YD-38 cells. In accordance, the expression of the BCL-2
      and BCL-XL, were inhibited, indicating the role of mitochondria in MSM-induced
      apoptosis. Analysis of mitochondrial integrity showed a loss of mitochondrial
      potential with an increased level of cytochrome c in the cytosol compared to
      mitochondria. Active CASPASE-3 (CASP3) was also observed, confirming that
      MSM-induced apoptosis is caspase-mediated.
CI  - Copyright(c) 2017, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - P, Nipin S
AU  - P NS
AD  - Department of Pathology, School of Medicine, Institute of Biomedical Science and 
      Technology, Konkuk University, Seoul, Republic of Korea.
FAU - Kang, Dong Young
AU  - Kang DY
AD  - Department of Pathology, School of Medicine, Institute of Biomedical Science and 
      Technology, Konkuk University, Seoul, Republic of Korea.
FAU - Kim, Baek Joong
AU  - Kim BJ
AD  - Department of Oral and Maxillofacial Surgery, College of Medicine, The Catholic
      University of Korea, Seoul, Republic of Korea.
FAU - Joung, Youn Hee
AU  - Joung YH
AD  - Department of Pathology, School of Medicine, Institute of Biomedical Science and 
      Technology, Konkuk University, Seoul, Republic of Korea.
FAU - Darvin, Pramod
AU  - Darvin P
AD  - Department of Pathology, School of Medicine, Institute of Biomedical Science and 
      Technology, Konkuk University, Seoul, Republic of Korea.
FAU - Byun, Hyo Joo
AU  - Byun HJ
AD  - Department of Pathology, School of Medicine, Institute of Biomedical Science and 
      Technology, Konkuk University, Seoul, Republic of Korea.
FAU - Kim, Joong Gon
AU  - Kim JG
AD  - Natural & Inc. Bando officetel, Busan, Republic of Korea.
FAU - Park, Je Uk
AU  - Park JU
AD  - Department of Oral and Maxillofacial Surgery, College of Medicine, The Catholic
      University of Korea, Seoul, Republic of Korea.
FAU - Yang, Young Mok
AU  - Yang YM
AD  - Department of Pathology, School of Medicine, Institute of Biomedical Science and 
      Technology, Konkuk University, Seoul, Republic of Korea [email protected]
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p21)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sulfones)
RN  - 9007-43-6 (Cytochromes c)
RN  - 9H4PO4Z4FT (dimethyl sulfone)
RN  - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases)
RN  - YOW8V9698H (Dimethyl Sulfoxide)
SB  - IM
MH  - Apoptosis/drug effects
MH  - Blotting, Western
MH  - Carcinoma, Squamous Cell/drug therapy/metabolism/*pathology
MH  - Cell Cycle Checkpoints/*drug effects
MH  - Cell Proliferation/drug effects
MH  - Cyclin-Dependent Kinase Inhibitor p21/genetics/metabolism
MH  - Cytochromes c/metabolism
MH  - Dimethyl Sulfoxide/*pharmacology
MH  - G1 Phase/*drug effects
MH  - Gingival Neoplasms/drug therapy/metabolism/*pathology
MH  - Humans
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Mitochondria/drug effects/metabolism/*pathology
MH  - Poly(ADP-ribose) Polymerases/genetics/metabolism
MH  - RNA, Messenger/genetics
MH  - Real-Time Polymerase Chain Reaction
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/drug effects
MH  - Sulfones/*pharmacology
MH  - Tumor Cells, Cultured
OTO - NOTNLM
OT  - *BAX-BCL-2
OT  - *CYC
OT  - *G1 arrest
OT  - *MSM
OT  - *mitochondrial apoptosis
EDAT- 2017/04/05 06:00
MHDA- 2017/04/14 06:00
CRDT- 2017/04/05 06:00
PHST- 2017/01/20 [received]
PHST- 2017/03/01 [revised]
PHST- 2017/03/02 [accepted]
AID - 37/4/1637 [pii]
AID - 10.21873/anticanres.11494 [doi]
PST - ppublish
SO  - Anticancer Res. 2017 Apr;37(4):1637-1646.

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