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Toll-like receptor 4 promotes proliferation and apoptosis resistance in human papillomavirus-related cervical cancer cells through the Toll-like receptor 4/nuclear factor-κB pathway.

Abstract Toll-like receptor 4 is overexpressed in various tumors, including cervical carcinoma. However, the role of Toll-like receptor 4 in cervical cancer remains controversial, and the underlying mechanisms are largely elusive. Therefore, Toll-like receptor 4 in cervical cancer and related mechanisms were investigated in this study. Quantitative reverse transcription polymerase chain reaction and western blot analyses were used to detect messenger RNA and protein levels in HeLa, Caski, and C33A cells with different treatments. Proliferation was quantified using Cell Counting Kit-8. Cell cycle distribution and apoptosis were assessed by flow cytometry. Higher levels of Toll-like receptor 4 expression were found in human papillomavirus-positive cells compared to human papillomavirus-negative cells. Proliferation of HeLa and Caski cells was promoted in lipopolysaccharide-stimulated groups but suppressed in short hairpin RNA-transfected groups. Apoptosis rates were lower in lipopolysaccharide-stimulated groups relative to short hairpin RNA-transfected groups. In addition, G2-phase distribution was enhanced when Toll-like receptor 4 was downregulated. Moreover, the pNF-κBp65 level was positively correlated with the Toll-like receptor 4 level in HeLa and Caski cells, though when an nuclear factor-κB inhibitor was applied to lipopolysaccharide-stimulated groups, the patterns of proliferation and apoptosis were opposite to those of the lipopolysaccharide-stimulated groups without inhibitor treatment. In conclusion, these data suggest that Toll-like receptor 4 promotes proliferation and apoptosis resistance in human papillomavirus-related cervical cancer cells at least in part through the Toll-like receptor 4/nuclear factor-κB pathway, which may be correlated with the occurrence and development of cervical carcinoma.
PMID
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Authors

Mayor MeshTerms
Keywords

Toll-like receptor 4

apoptosis

cervical cancer

human papillomavirus

nuclear factor-κB

proliferation

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28653898
OWN - NLM
STAT- MEDLINE
DA  - 20170627
DCOM- 20170711
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Toll-like receptor 4 promotes proliferation and apoptosis resistance in human
      papillomavirus-related cervical cancer cells through the Toll-like receptor
      4/nuclear factor-kappaB pathway.
PG  - 1010428317710586
LID - 10.1177/1010428317710586 [doi]
AB  - Toll-like receptor 4 is overexpressed in various tumors, including cervical
      carcinoma. However, the role of Toll-like receptor 4 in cervical cancer remains
      controversial, and the underlying mechanisms are largely elusive. Therefore,
      Toll-like receptor 4 in cervical cancer and related mechanisms were investigated 
      in this study. Quantitative reverse transcription polymerase chain reaction and
      western blot analyses were used to detect messenger RNA and protein levels in
      HeLa, Caski, and C33A cells with different treatments. Proliferation was
      quantified using Cell Counting Kit-8. Cell cycle distribution and apoptosis were 
      assessed by flow cytometry. Higher levels of Toll-like receptor 4 expression were
      found in human papillomavirus-positive cells compared to human
      papillomavirus-negative cells. Proliferation of HeLa and Caski cells was promoted
      in lipopolysaccharide-stimulated groups but suppressed in short hairpin
      RNA-transfected groups. Apoptosis rates were lower in
      lipopolysaccharide-stimulated groups relative to short hairpin RNA-transfected
      groups. In addition, G2-phase distribution was enhanced when Toll-like receptor 4
      was downregulated. Moreover, the pNF-kappaBp65 level was positively correlated
      with the Toll-like receptor 4 level in HeLa and Caski cells, though when an
      nuclear factor-kappaB inhibitor was applied to lipopolysaccharide-stimulated
      groups, the patterns of proliferation and apoptosis were opposite to those of the
      lipopolysaccharide-stimulated groups without inhibitor treatment. In conclusion, 
      these data suggest that Toll-like receptor 4 promotes proliferation and apoptosis
      resistance in human papillomavirus-related cervical cancer cells at least in part
      through the Toll-like receptor 4/nuclear factor-kappaB pathway, which may be
      correlated with the occurrence and development of cervical carcinoma.
FAU - Jiang, Ninghong
AU  - Jiang N
AD  - 1 Medical Center of Diagnosis and Treatment for Cervical Diseases, Obstetrics and
      Gynecology Hospital of Fudan University, Shanghai, China.
AD  - 2 Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,
      Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
FAU - Xie, Feng
AU  - Xie F
AD  - 1 Medical Center of Diagnosis and Treatment for Cervical Diseases, Obstetrics and
      Gynecology Hospital of Fudan University, Shanghai, China.
AD  - 2 Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,
      Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
FAU - Guo, Qisang
AU  - Guo Q
AD  - 1 Medical Center of Diagnosis and Treatment for Cervical Diseases, Obstetrics and
      Gynecology Hospital of Fudan University, Shanghai, China.
AD  - 2 Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,
      Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
FAU - Li, Ming-Qing
AU  - Li MQ
AD  - 2 Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,
      Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
FAU - Xiao, Jingjing
AU  - Xiao J
AD  - 1 Medical Center of Diagnosis and Treatment for Cervical Diseases, Obstetrics and
      Gynecology Hospital of Fudan University, Shanghai, China.
AD  - 2 Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,
      Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
FAU - Sui, Long
AU  - Sui L
AD  - 1 Medical Center of Diagnosis and Treatment for Cervical Diseases, Obstetrics and
      Gynecology Hospital of Fudan University, Shanghai, China.
AD  - 2 Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,
      Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (NF-kappa B)
RN  - 0 (RELA protein, human)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Transcription Factor RelA)
SB  - IM
MH  - Apoptosis/genetics
MH  - Cell Proliferation/genetics
MH  - Female
MH  - Flow Cytometry
MH  - Gene Expression Regulation, Neoplastic
MH  - HeLa Cells
MH  - Humans
MH  - NF-kappa B/*genetics
MH  - Papillomaviridae/genetics/pathogenicity
MH  - Toll-Like Receptor 4/biosynthesis/*genetics
MH  - Transcription Factor RelA/*biosynthesis/genetics
MH  - Uterine Cervical Neoplasms/*genetics/pathology/virology
OTO - NOTNLM
OT  - Toll-like receptor 4
OT  - apoptosis
OT  - cervical cancer
OT  - human papillomavirus
OT  - nuclear factor-kappaB
OT  - proliferation
EDAT- 2017/06/28 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/28 06:00
AID - 10.1177/1010428317710586 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317710586. doi: 10.1177/1010428317710586.