PIG3 promotes NSCLC cell mitotic progression and is associated with poor prognosis of NSCLC patients

Ming Li, Shanhu Li, Biao Liu, Meng Meng Gu, Shitao Zou, Bei Bei Xiao, Lan Yu, Wei Qun Ding, Ping Kun Zhou, Jundong Zhou, Zeng Fu Shang

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background: Non-small cell lung cancer (NSCLC) is the most commonly diagnosed type of lung cancer that is associated with poor prognosis. In this study we explored the potential role of p53-induced gene 3 (PIG3) in the progression of NSCLC. Methods: Immunohistochemistry was used to determine the expression levels of PIG3 in 201 NSCLC patients. We performed in vitro studies and silenced endogenous PIG3 by using specific siRNAs that specific target PIG3. Immunofluorescent staining was performed to determine the effect of PIG3 on mitotic progression in NSCLC cells. The growth rates of microtubules were determined by microtubule nucleation analysis. Cell proliferation and chemosensitivity were analyzed by CCK8 assays. Annexin V staining and β-galactosidase activity analysis were used to evaluate PIG3 deficiency-related apoptosis and senescence, respectively. Results: PIG3 expression levels negatively correlated with overall survival and disease-free survival of NSCLC patients. Knock down of PIG3 resulted in repressed proliferation of NSCLC cells and increased aberrant mitosis, which included misaligning and lagging chromosomes, and bi- or multi-nucleated giant cells. In addition, PIG3 contributed to mitotic spindle assembly by promoting microtubule growth. Furthermore, loss of PIG3 sensitized NSCLC cells to docetaxel by enhancing docetaxel-induced apoptosis and senescence. Conclusions: Our results indicate that PIG3 promotes NSCLC progression and therefore suggest that PIG3 may be a potential prognostic biomarker and novel therapeutic target for the treatment of NSCLC.

Original languageEnglish (US)
Article number39
JournalJournal of Experimental and Clinical Cancer Research
Volume36
Issue number1
DOIs
StatePublished - Mar 4 2017

Fingerprint

p53 Genes
Non-Small Cell Lung Carcinoma
docetaxel
Microtubules
Galactosidases
Apoptosis
Staining and Labeling
Spindle Apparatus
Annexin A5
Giant Cells
Growth
Mitosis
Disease-Free Survival
Lung Neoplasms
Chromosomes
Biomarkers
Immunohistochemistry
Cell Proliferation

Keywords

  • Chemoresistance
  • Microtubule assembly
  • Mitotic progression
  • Non-small cell lung cancer (NSCLC)
  • p53-induced gene 3 (PIG3)

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

PIG3 promotes NSCLC cell mitotic progression and is associated with poor prognosis of NSCLC patients. / Li, Ming; Li, Shanhu; Liu, Biao; Gu, Meng Meng; Zou, Shitao; Xiao, Bei Bei; Yu, Lan; Ding, Wei Qun; Zhou, Ping Kun; Zhou, Jundong; Shang, Zeng Fu.

In: Journal of Experimental and Clinical Cancer Research, Vol. 36, No. 1, 39, 04.03.2017.

Research output: Contribution to journalArticle

Li, Ming ; Li, Shanhu ; Liu, Biao ; Gu, Meng Meng ; Zou, Shitao ; Xiao, Bei Bei ; Yu, Lan ; Ding, Wei Qun ; Zhou, Ping Kun ; Zhou, Jundong ; Shang, Zeng Fu. / PIG3 promotes NSCLC cell mitotic progression and is associated with poor prognosis of NSCLC patients. In: Journal of Experimental and Clinical Cancer Research. 2017 ; Vol. 36, No. 1.
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abstract = "Background: Non-small cell lung cancer (NSCLC) is the most commonly diagnosed type of lung cancer that is associated with poor prognosis. In this study we explored the potential role of p53-induced gene 3 (PIG3) in the progression of NSCLC. Methods: Immunohistochemistry was used to determine the expression levels of PIG3 in 201 NSCLC patients. We performed in vitro studies and silenced endogenous PIG3 by using specific siRNAs that specific target PIG3. Immunofluorescent staining was performed to determine the effect of PIG3 on mitotic progression in NSCLC cells. The growth rates of microtubules were determined by microtubule nucleation analysis. Cell proliferation and chemosensitivity were analyzed by CCK8 assays. Annexin V staining and β-galactosidase activity analysis were used to evaluate PIG3 deficiency-related apoptosis and senescence, respectively. Results: PIG3 expression levels negatively correlated with overall survival and disease-free survival of NSCLC patients. Knock down of PIG3 resulted in repressed proliferation of NSCLC cells and increased aberrant mitosis, which included misaligning and lagging chromosomes, and bi- or multi-nucleated giant cells. In addition, PIG3 contributed to mitotic spindle assembly by promoting microtubule growth. Furthermore, loss of PIG3 sensitized NSCLC cells to docetaxel by enhancing docetaxel-induced apoptosis and senescence. Conclusions: Our results indicate that PIG3 promotes NSCLC progression and therefore suggest that PIG3 may be a potential prognostic biomarker and novel therapeutic target for the treatment of NSCLC.",
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AU - Liu, Biao

AU - Gu, Meng Meng

AU - Zou, Shitao

AU - Xiao, Bei Bei

AU - Yu, Lan

AU - Ding, Wei Qun

AU - Zhou, Ping Kun

AU - Zhou, Jundong

AU - Shang, Zeng Fu

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AB - Background: Non-small cell lung cancer (NSCLC) is the most commonly diagnosed type of lung cancer that is associated with poor prognosis. In this study we explored the potential role of p53-induced gene 3 (PIG3) in the progression of NSCLC. Methods: Immunohistochemistry was used to determine the expression levels of PIG3 in 201 NSCLC patients. We performed in vitro studies and silenced endogenous PIG3 by using specific siRNAs that specific target PIG3. Immunofluorescent staining was performed to determine the effect of PIG3 on mitotic progression in NSCLC cells. The growth rates of microtubules were determined by microtubule nucleation analysis. Cell proliferation and chemosensitivity were analyzed by CCK8 assays. Annexin V staining and β-galactosidase activity analysis were used to evaluate PIG3 deficiency-related apoptosis and senescence, respectively. Results: PIG3 expression levels negatively correlated with overall survival and disease-free survival of NSCLC patients. Knock down of PIG3 resulted in repressed proliferation of NSCLC cells and increased aberrant mitosis, which included misaligning and lagging chromosomes, and bi- or multi-nucleated giant cells. In addition, PIG3 contributed to mitotic spindle assembly by promoting microtubule growth. Furthermore, loss of PIG3 sensitized NSCLC cells to docetaxel by enhancing docetaxel-induced apoptosis and senescence. Conclusions: Our results indicate that PIG3 promotes NSCLC progression and therefore suggest that PIG3 may be a potential prognostic biomarker and novel therapeutic target for the treatment of NSCLC.

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