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STC1 promotes cell apoptosis via NF-κB phospho-P65 Ser536 in cervical cancer cells

Xi Pan1,2,3, Binyuan Jiang1,2, Jianhao Liu4

  • 1The Key Laboratory of Carcinogenesis of The Chinese Ministry of Health and The Key Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha 410008, China.

Oncotarget
|May 26, 2017
PubMed

Insights

Stanniocalin-1 (STC1) promotes cervical cancer cell apoptosis by activating NF-κB P65 phosphorylation through the PI3K/AKT pathway. This study elucidates STC1's mechanism in regulating apoptosis and cell growth in cervical cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Stanniocalin-1 (STC1) is implicated in human malignancies, with prior research suggesting it inhibits cervical cancer cell proliferation and invasion via NF-κB P65 activation.
  • The precise mechanism by which STC1 influences cervical cancer progression and apoptosis remains incompletely understood.

Purpose of the Study:

  • To investigate the role of STC1 in cervical cancer cell apoptosis and elucidate its underlying molecular mechanisms.
  • To determine the relationship between STC1 expression and key signaling pathways involved in cell growth and apoptosis.

Main Methods:

  • Overexpression and silencing of STC1 in cervical cancer cells.
  • Phospho-protein profiling and Western blotting to analyze protein expression and phosphorylation.
  • Utilizing PI3K inhibitor (LY294002), AKT-shRNA, and IκBα-shRNA to probe signaling pathways.
  • Flow cytometry to assess apoptosis and cell cycle progression.
  • Immunohistochemistry on cervical cancer microarrays to correlate STC1 and signaling protein levels with clinical stages.

Main Results:

  • Overexpression of STC1 promoted apoptosis, while STC1 silencing enhanced cell growth in cervical cancer.
  • STC1 altered the phosphorylation status of NF-κB P65 (Ser536), IκBα, IKKβ, PI3K, and AKT.
  • Inhibition of PI3K/AKT or IκBα pathways reversed STC1-induced changes in NF-κB phosphorylation and increased apoptosis.
  • STC1 levels were decreased in cervical cancer tissues, particularly in stages II and III, with lower STC1 and phospho-PI3K but higher phospho-P65 in tumors compared to normal tissues.

Conclusions:

  • STC1 promotes cervical cancer cell apoptosis by activating NF-κB P65 phosphorylation at Ser536 via the PI3K/AKT and IKK/IκBα signaling pathways.
  • STC1 plays a suppressive role in cervical cancer progression, and its reduced expression in advanced stages suggests a potential tumor-suppressive function.
  • These findings provide the first mechanistic explanation for STC1's role in regulating apoptosis in cervical cancer.
Keywords:
NF-κBcell apoptosiscervical cancerphospho-P65 (Ser536)stanniocalin-1 (STC1)

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