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. 2022 Mar 11:2022:1091042.
doi: 10.1155/2022/1091042. eCollection 2022.

PTPN18 Stimulates the Development of Ovarian Cancer by Activating the PI3K/AKT Signaling

Nan Mao  1 , Hu Li  2 , Hui Yang  1 , Jianfen Su  1 , Zhimin Liang  1 , Guansheng He  3
Affiliations

PTPN18 Stimulates the Development of Ovarian Cancer by Activating the PI3K/AKT Signaling

Nan Mao et al. Evid Based Complement Alternat Med. .

Retraction in

Abstract

Objective: To illustrate the functions of protein tyrosine phosphatase nonreceptor type 18 (PTPN18) in the progression of ovarian cancer and the potential molecular mechanism.

Methods: Differential PTPN18 expression in ovarian cancer samples was determined. Following PTPN18 knockdown, changes in proliferation and migration in ovarian cancer cells were detected. Nude mice with ovarian cancer were used to uncover the effects of PTPN18 on ovarian cancer growth in vivo.

Results: PTPN18 was significantly upregulated in ovarian cancer samples and linked to pathological staging and metastasis rate. PTPN18 displayed prognostic and diagnostic potentials in ovarian cancer. Knockdown of PTPN18 and treatment of the PI3K inhibitor could inhibit proliferative and migratory abilities in ovarian cancer cells. Moreover, PTPN18 was capable of inactivating PI3K/AKT signaling. In vivo knockdown of PTPN18 suppressed ovarian cancer growth in nude mice.

Conclusions: PTPN18 is upregulated in ovarian cancer, which stimulates the malignant development by activating PI3K/AKT signaling. The PTPN18 level is also associated with pathological staging and metastasis in ovarian cancer patients, which may be utilized as a hallmark predicting the malignant level.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1
Upregulation of PTPN18 in ovarian cancer samples. (a) Differential expression of PTPN18 in OC tissues and paracancerous ones. (b) PTPN18 level in ovarian cancer cell lines. (c) Overall survival in ovarian cancer patients based on their PTPN18 level. (d) ROC curves showing specificity and sensitivity in diagnostic potential of PTPN18 in ovarian cancer. (e) Transfection efficacy of sh-PTPN18#1 and sh-PTPN18#2 in A2780 and CAOV3 cells. Data are expressed as mean ± SD. ∗∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.
Figure 2
Figure 2
PTPN18 knockdown inhibited proliferation and migration of OC. (a) Viability in A2780 and CAOV3 cells transfected with sh-NC, sh-PTPN18#1, or sh-PTPN18#2, respectively. (b) Migration in A2780 and CAOV3 cells with sh-PTPN18#1, sh-PTPN18#2, or sh-NC, respectively (magnification: 40×). ∗P < 0.05.
Figure 3
Figure 3
Knockdown of PTPN18 inactivated PI3K/AKT signaling in ovarian cancer. (a) Protein levels of p-AKT, AKT, p-mTOR, p-PI3K, PI3K, and mTOR in A2780 and CAOV3 cells transfected with sh-NC, sh-PTPN18#1, or sh-PTPN18#2, respectively. (b) Protein level of PTPN18 in A2780 and CAOV3 cells induced with LY294002. (c) Viability in A2780 and CAOV3 cells induced with LY294002. (d) Migration in A2780 and CAOV3 cells induced with LY294002. ∗P < 0.05, ∗∗P < 0.01.
Figure 4
Figure 4
PTPN18 knockdown inhibited tumorigenesis of ovarian cancer. (a) Tumor volume that was weekly recorded in nude mice administrated with A2780 cells transfected with sh-NC or sh-PTPN18#1. (b) Tumor weight in nude mice administrated with A2780 cells transfected with sh-NC or sh-PTPN18#1. (c) Protein level of PTPN18 in ovarian cancer tissues collected from nude mice administrated with A2780 cells transfected with sh-NC or sh-PTPN18#1. (d) Positive level of PTPN18 in ovarian cancer tissues collected from nude mice administrated with A2780 cells transfected with sh-NC or sh-PTPN18#1. ∗P < 0.05, ∗∗P < 0.01.
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