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TIPE2 suppressed cisplatin resistance by inducing autophagy via mTOR signalling pathway

Hua Guo1, Hui Ren2, Jie Li3

  • 1The department of Respiratory and Critical Care Medicine, Xi'an Central Hospital, The Affiliated Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710003, China.

Experimental and Molecular Pathology
|January 10, 2020
PubMed

Insights

Tumour necrosis factor-α-induced protein-8-like-2 (TIPE2) is down-regulated in cisplatin-resistant non-small-cell lung cancer (NSCLC). Restoring TIPE2 enhances cisplatin sensitivity by modulating autophagy via the mTOR pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Tumour necrosis factor-α-induced protein-8-like-2 (TIPE2) is implicated in cancer progression.
  • Cisplatin resistance is a significant challenge in non-small-cell lung cancer (NSCLC) therapy.

Purpose of the Study:

  • To investigate the role of TIPE2 in cisplatin resistance in NSCLC.
  • To elucidate the molecular mechanisms underlying TIPE2's function in chemoresistance.

Main Methods:

  • Comparative analysis of TIPE2 expression in cisplatin-resistant versus sensitive NSCLC tissues and cells.
  • Functional studies involving TIPE2 inhibition and overexpression.
  • Investigation of autophagy and mTOR signaling pathway activity.

Main Results:

  • TIPE2 was significantly down-regulated in cisplatin-resistant NSCLC.
  • TIPE2 inhibition promoted cisplatin resistance, while TIPE2 overexpression enhanced sensitivity, apoptosis, and autophagy.
  • TIPE2 modulated autophagy through the mTOR signaling pathway, which was confirmed by experiments with an mTOR activator.

Conclusions:

  • Aberrant TIPE2 expression contributes to cisplatin chemoresistance in NSCLC by regulating autophagy in an mTOR-dependent manner.
  • TIPE2 represents a potential therapeutic target for overcoming cisplatin resistance in NSCLC.

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