Fra-1 is upregulated in gastric cancer tissues and affects the PI3K/Akt and p53 signaling pathway in gastric cancer.
Gastric cancer is an aggressive disease that continues to have a daunting impact on global health. Fra-1 (FOSL1) plays important roles in oncogenesis in various malignancies. We investigated the expression of Fra-1 in gastric cancer (GC) tissues by qPCR, immunohistochemistry (IHC) and western blot technologies. The results showed that Fra-1 was overexpressed in gastric cancer tissues compared with the adjacent non‑cancerous tissues. To explore the possible mechanism of Fra-1 in GC, we elucidated the effect of Fra-1 in the apoptosis and cell cycle of gastric cancer cells, AGS, and found that a considerable decrease in apoptotic cells and increase of S phase rate were observed for AGS cells with Fra-1 overexpession. We identified and confirmed that Fra-1 affected the expression level of CTTN and EZR in vitro through LC-MS/MS analyses and western blot technology. Furthermore, we found that Fra-1 was correlated with dysregulation PI3K/Akt and p53 signaling pathway in gastric cancer tissues in vitro. Moreover, we found that Fra-1 overexpression affected the expression of PI3K, Akt, MDM2 and p53 in vivo. In summary, our results suggest that Fra-1 is upregulated in gastric cancer tissues and plays its function by affecting the PI3K/Akt and p53 signaling pathway in gastric cancer.
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Junyu
J
He
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Guangchao
G
Zhu
Cancer Research Institute, Central South University, Changsha, Hunan 410078, P.R. China.
Lu
L
Gao
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Pan
P
Chen
Cancer Research Institute, Central South University, Changsha, Hunan 410078, P.R. China.
Yuehua
Y
Long
Cancer Research Institute, Central South University, Changsha, Hunan 410078, P.R. China.
Shan
S
Liao
Research Center of Carcinogenesis and Targeted Therapy, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Hong
H
Yi
Cancer Research Institute, Central South University, Changsha, Hunan 410078, P.R. China.
Wei
W
Yi
Cancer Research Institute, Central South University, Changsha, Hunan 410078, P.R. China.
Zhen
Z
Pei
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Minghua
M
Wu
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Xiaoling
X
Li
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Juanjuan
J
Xiang
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Shuping
S
Peng
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Jian
J
Ma
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Ming
M
Zhou
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Wei
W
Xiong
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Zhaoyang
Z
Zeng
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Bo
B
Xiang
Cancer Research Institute, Central South University, Changsha, Hunan 410078, P.R. China.
Ke
K
Tang
Cancer Research Institute, Central South University, Changsha, Hunan 410078, P.R. China.
Li
L
Cao
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Guiyuan
G
Li
Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410006, P.R. China.
Yanhong
Y
Zhou
D017209:Apoptosis / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics; D051356:Cortactin / Q000096:biosynthesis* / Q000235:genetics; D003598:Cytoskeletal Proteins / Q000096:biosynthesis* / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000096:biosynthesis; D051057:Proto-Oncogene Proteins c-akt / Q000096:biosynthesis; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis* / Q000235:genetics; D013274:Stomach Neoplasms / Q000235:genetics* / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis; D000099149:Ezrin; D000099169:Fos-Related Antigen 1
D051356:Cortactin; D003598:Cytoskeletal Proteins; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D016760:Proto-Oncogene Proteins c-fos; D016159:Tumor Suppressor Protein p53; D000099149:Ezrin; D000099169:Fos-Related Antigen 1; C495868:CTTN protein, human