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TIPE1-mediated autophagy suppression promotes nasopharyngeal carcinoma cell proliferation via the AMPK/mTOR

Yongliang Liu¹, Xiangqin Qi², Zhenan Zhao¹

¹Department of Otolaryngolgogy, Zibo Central Hospital, Shandong University, Zibo, China.

Journal of Cellular and Molecular Medicine

|June 27, 2020

Abstract:

Recent studies have shown that tumour necrosis factor-α-induced protein 8 like-1(TIPE1) plays distinct roles in different cancers. TIPE1 inhibits tumour proliferation and metastasis in a variety of tumours but acts as an oncogene in cervical cancer. The role of TIPE1 in nasopharyngeal carcinoma (NPC) remains unknown. Interestingly, TIPE1 expression was remarkably increased in NPC tissue samples compared to adjacent normal nasopharyngeal epithelial tissue samples in our study. TIPE1 expression was positively correlated with that of the proliferation marker Ki67 and negatively correlated with patient lifespan. In vitro, TIPE1 inhibited autophagy and induced cell proliferation in TIPE1-overexpressing CNE-1 and CNE-2Z cells. In addition, knocking down TIPE1 expression promoted autophagy and decreased proliferation, whereas overexpressing TIPE1 increased the levels of pmTOR, pS6 and P62 and decreased the level of pAMPK and the LC3B. Furthermore, the decrease in autophagy was remarkably rescued in TIPE1-overexpressing CNE-1 and CNE-2Z cells treated with the AMPK activator AICAR. In addition, TIPE1 promoted tumour growth in BALB/c nude mice. Taken together, results indicate that TIPE1 promotes NPC progression by inhibiting autophagy and inducing cell proliferation via the AMPK/mTOR signalling pathway. Thus, TIPE1 could potentially be used as a valuable diagnostic and prognostic biomarker for NPC.

Insights

Tumour necrosis factor-α-induced protein 8 like-1 (TIPE1) promotes nasopharyngeal carcinoma (NPC) progression by inhibiting autophagy and inducing cell proliferation. TIPE1 may serve as a diagnostic and prognostic biomarker for NPC.

Area of Science:

Oncology
Molecular Biology
Cancer Research

Background:

Tumour necrosis factor-α-induced protein 8 like-1 (TIPE1) has varied roles in different cancers.
Its function in nasopharyngeal carcinoma (NPC) was previously unknown.

Purpose of the Study:

To investigate the role of TIPE1 in nasopharyngeal carcinoma (NPC).
To explore the underlying molecular mechanisms of TIPE1 in NPC progression.

Main Methods:

Analysis of TIPE1 expression in NPC tissues and its correlation with clinical parameters.
In vitro studies using NPC cell lines (CNE-1, CNE-2Z) to assess the effects of TIPE1 on cell proliferation and autophagy.
Investigation of the involvement of the AMPK/mTOR signaling pathway.
In vivo studies using a mouse model.

Main Results:

TIPE1 expression is upregulated in NPC tissues and correlates with increased proliferation (Ki67) and decreased patient survival.
TIPE1 overexpression inhibits autophagy and promotes cell proliferation in NPC cells, while TIPE1 knockdown has the opposite effect.
TIPE1 influences the AMPK/mTOR pathway by affecting levels of pmTOR, pS6, P62, and pAMPK.
TIPE1 promotes tumour growth in vivo.
Autophagy inhibition by TIPE1 can be rescued by AICAR, an AMPK activator.

Conclusions:

TIPE1 promotes NPC progression by inhibiting autophagy and inducing cell proliferation through the AMPK/mTOR signaling pathway.
TIPE1 is a potential diagnostic and prognostic biomarker for NPC.

Read full analysis

Keywords:

AMPK/mTOR signalling pathway TIPE1 autophagy cell proliferation nasopharyngeal carcinoma

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