PMID- 35156537
OWN - NLM
STAT- MEDLINE
DCOM- 20220408
LR  - 20220531
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 3
DP  - 2022 Mar
TI  - Ribophorin II promotes the epithelial-mesenchymal transition and aerobic 
      glycolysis of laryngeal squamous cell carcinoma via regulating reactive oxygen 
      species-mediated Phosphatidylinositol-3-Kinase/Protein Kinase B activation.
PG  - 5141-5151
LID - 10.1080/21655979.2022.2036914 [doi]
AB  - Ribophorin II (RPN2), a part of an N-oligosaccharyl transferase complex, plays 
      vital roles in the development of multiple cancers. Nevertheless, its biological 
      role in laryngeal squamous cell carcinoma (LSCC) remains unclear. The RPN2 
      expression levels in LSCC tissues and cell lines (AMC-HN-8 and TU212) were 
      measured using real-time PCR, immunohistochemistry, or Western blot. The 
      influences of RPN2 on the proliferation, migration, epithelial-mesenchymal 
      transition, and aerobic glycolysis of LSCC cells were investigated after 
      upregulation or downregulation of RPN2 in vitro and in vivo. Mechanically, we 
      assessed the impact of RPN2 on the reactive oxygen species 
      (ROS)/Phosphatidylinositol-3-Kinase (PI3K)/Protein Kinase B (Akt) signaling 
      pathway. We found that compared with the control, RPN2 was highly expressed in 
      LSCC tissues and cells. Overexpression of RPN2 elevated the proliferation, 
      migration, glucose uptake, lactate production release, and levels of Vimentin, 
      hexokinase-2 (HK-2), pyruvate dehydrogenase kinase 1 (PDK1), lactate 
      dehydrogenase A (LDHA), and ROS, but inhibited E-cadherin expression in AMC-HN-8 
      cells. Knockdown of RPN2 in TU212 cells showed opposite effects on the above 
      indexes. Meanwhile, RPN2 upregulation increased the levels of p-PI3K/PI3K and 
      p-Akt/Akt, which were attenuated by N-acetyl-L-cysteine (NAC), an ROS inhibitor. 
      Both NAC and PI3K inhibitor LY294002 could reverse the effects of RPN2 
      overexpression on the malignant phenotypes of LSCC cells. In xenografted mice, 
      silencing RPN2 expression reduced tumor growth, ROS production, and levels of 
      Ki-67, Vimentin, LDHA, and p-Akt/Akt, but enhanced E-cadherin expression. In 
      conclusion, our data suggested that RPN2 promoted the proliferation, migration, 
      EMT, and glycolysis of LSCC via modulating ROS-mediated PI3K/Akt activation.
FAU - Zhou, Jingchun
AU  - Zhou J
AD  - Department of Otorhinolaryngology, Shenzhen People's Hospital (The Second 
      Clinical Medical College, Jinan University; The First Affiliated Hospital, 
      Southern University of Science and Technology), Shenzhen, Guangdong, China.
FAU - Zhang, Jingjing
AU  - Zhang J
AD  - Department of Otorhinolaryngology, Peking University Shenzhen Hospital, Shenzhen, 
      China.
FAU - Zhang, Wei
AU  - Zhang W
AD  - Department of Otorhinolaryngology, Shenzhen People's Hospital (The Second 
      Clinical Medical College, Jinan University; The First Affiliated Hospital, 
      Southern University of Science and Technology), Shenzhen, Guangdong, China.
FAU - Ke, Zhaoyang
AU  - Ke Z
AD  - Department of Otorhinolaryngology, Shenzhen People's Hospital (The Second 
      Clinical Medical College, Jinan University; The First Affiliated Hospital, 
      Southern University of Science and Technology), Shenzhen, Guangdong, China.
FAU - Lv, Yanlu
AU  - Lv Y
AD  - Department of Otorhinolaryngology, Shenzhen People's Hospital (The Second 
      Clinical Medical College, Jinan University; The First Affiliated Hospital, 
      Southern University of Science and Technology), Shenzhen, Guangdong, China.
FAU - Zhang, Bo
AU  - Zhang B
AD  - Department of Otorhinolaryngology, Shenzhen People's Hospital (The Second 
      Clinical Medical College, Jinan University; The First Affiliated Hospital, 
      Southern University of Science and Technology), Shenzhen, Guangdong, China.
FAU - Liao, Zhifang
AU  - Liao Z
AD  - Department of Otorhinolaryngology, Shenzhen People's Hospital (The Second 
      Clinical Medical College, Jinan University; The First Affiliated Hospital, 
      Southern University of Science and Technology), Shenzhen, Guangdong, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (Cadherins)
RN  - 0 (Phosphatidylinositols)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Vimentin)
RN  - EC 2.4.1.- (Hexosyltransferases)
RN  - EC 2.4.99.18 (RPN2 protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 3.4.25.1 (Proteasome Endopeptidase Complex)
SB  - IM
MH  - Animals
MH  - Cadherins/genetics/metabolism
MH  - Cell Line, Tumor
MH  - Cell Proliferation/genetics
MH  - *Epithelial-Mesenchymal Transition
MH  - Glycolysis/genetics
MH  - *Hexosyltransferases/genetics
MH  - Humans
MH  - *Laryngeal Neoplasms/pathology
MH  - Mice
MH  - Phosphatidylinositol 3-Kinases/genetics/metabolism
MH  - Phosphatidylinositols
MH  - *Proteasome Endopeptidase Complex/genetics
MH  - Proto-Oncogene Proteins c-akt/genetics/metabolism
MH  - Reactive Oxygen Species
MH  - *Squamous Cell Carcinoma of Head and Neck/pathology
MH  - Vimentin/metabolism
PMC - PMC8974210
OTO - NOTNLM
OT  - EMT
OT  - ROS/PI3K/AKT
OT  - RPN2
OT  - aerobic glycolysis
OT  - laryngeal squamous cell carcinoma
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/02/15 06:00
MHDA- 2022/04/09 06:00
PMCR- 2022/02/14
CRDT- 2022/02/14 08:52
PHST- 2022/02/14 08:52 [entrez]
PHST- 2022/02/15 06:00 [pubmed]
PHST- 2022/04/09 06:00 [medline]
PHST- 2022/02/14 00:00 [pmc-release]
AID - 2036914 [pii]
AID - 10.1080/21655979.2022.2036914 [doi]
PST - ppublish
SO  - Bioengineered. 2022 Mar;13(3):5141-5151. doi: 10.1080/21655979.2022.2036914.