scholarly journals Elevated expression of FABP3 and FABP4 cooperatively correlates with poor prognosis in non-small cell lung cancer (NSCLC)

Oncotarget ◽  
2016 ◽  
Vol 7 (29) ◽  
pp. 46253-46262 ◽  
Author(s):  
Zhiyuan Tang ◽  
Qin Shen ◽  
Hao Xie ◽  
Xiaoyu Zhou ◽  
Jun Li ◽  
...  
2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Qiuyuan Wen ◽  
Yuting Zhan ◽  
Hongmei Zheng ◽  
Hongjing Zang ◽  
Jiadi Luo ◽  
...  

Abstract Background Mcl-1, an anti-apoptotic member of bcl-2 family, together with cleaved poly (ADC-ribose) polymerase (c-PARP) can serve as a marker of cell apoptosis. Previously we reported that treatment of Mnk inhibitor CGP57380 resulted in decreased Mcl-1 expression while increased c-PARP expression in non-small cell lung cancer (NSCLC) cells. In this study, we aimed to investigate association between Mcl-1 expression and clinicopathological features of NSCLC, and their correlation between Mcl-1 and both proliferation index (PI) and apoptotic index (AI) in NSCLC patients. Methods Tissue microarrays (TMA) including 350 cases of surgically resected NSCLC were utilize and stained with Mcl-1, Ki-67 and c-PARP antibodies, PI and AI were then evaluated, respectively. Results Higher Mcl-1 expression and PI were observed in NSCLC compared with non-cancerous lung tissues (non-CLT), while AI was significantly lower in lung adenocarcinoma (ADC) compared with non-CLT. Additionally, Mcl-1 expression in lung ADC was evidently higher than that of in lung squamous cell carcinoma (SCC). The elevated Mcl-1 expression was associated with PI, and inversely related to AI in NSCLC. NSCLC patients with elevated Mcl-1 expression and high PI, or with high Mcl-1 expression and low AI had remarkably shorter overall survival time than these patients with low Mcl-1 expression. Conclusions Elevated expression of Mcl-1 might be inversely proportional to disease progression of NSCLC patients by promoting cell proliferation and inhibiting apoptosis, and Mcl-1 might serve as novel biomarker of poor prognosis for NSCLC patients.


Tumor Biology ◽  
2014 ◽  
Vol 35 (9) ◽  
pp. 8673-8678 ◽  
Author(s):  
Chun-Hua Xu ◽  
Zhi-Hong Sheng ◽  
Hui-Di Hu ◽  
Ke-Ke Hao ◽  
Qing-Bo Wang ◽  
...  

2018 ◽  
Vol 64 (4) ◽  
pp. 522-527
Author(s):  
Aleksey Shutko ◽  
Viktor Mus

Individual parameters of circulating hemopoietic stem cells (HSC) lymphoid origin were measured by cytofluorometry before treatment of patients with metastatic non-small cell lung cancer and were retrospectively compared with individual life span's (LS). The possibility of poor prognosis of treatment's results (LS


Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 3426-3433
Author(s):  
Juanjuan Yong ◽  
Liyun Huang ◽  
Gengbiao Chen ◽  
Xiaoya Luo ◽  
Hui Chen ◽  
...  

2017 ◽  
Vol 14 (4) ◽  
pp. 3959-3966 ◽  
Author(s):  
Dan Liu ◽  
Yi Huang ◽  
Li Zhang ◽  
Dong-Ni Liang ◽  
Li Li

2018 ◽  
Vol 45 (6) ◽  
pp. 2213-2224 ◽  
Author(s):  
Meng Zhao ◽  
Yahui Liu ◽  
Ran Liu ◽  
Jin Qi ◽  
Yongwang Hou ◽  
...  

Background/Aims: Cytokines are key players in tumorigenesis and are potential targets in cancer treatment. Although IL-6 has attracted considerable attention, interleukin 11 (IL-11), another member of the IL-6 family, has long been overlooked, and little is known regarding its specific function in non-small cell lung cancer (NSCLC). In this study, we explored IL-11’s role in NSCLC and the detailed mechanism behind it. Methods: Cell proliferation in response to IL-11 was determined by colony formation, BrdU incorporation and MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay. Cell motility was measured by Transwell and wound healing assays. NSCLC xenograft models were used to confirm oncogenic function of IL-11 in vivo. Immunohistochemical staining and western blot assay were performed to detect epithelial–mesenchymal transition (EMT) markers and cell signaling pathway alterations. Eighteen NSCLC patients and 5 normal lung samples were collected together with data from an online database to determine the link between IL-11 expression and malignant progression. Results: We observed that IL-11 was upregulated in NSCLC samples compared with normal tissue samples and correlated with poor prognosis. Data from in vitro and in vivo models indicated that IL-11 promotes cell proliferation and tumorigenesis. Cell migration and invasion were also enhanced by IL-11. Epithelial–mesenchymal transition (EMT) was also observed after IL-11 incubation. Furthermore, IL-11 activated AKT and STAT3 in our experimental models. In addition, we observed that hypoxia induced IL-11 expression in NSCLC cells. Deferoxamine (DFX) or dimethyloxalylglycine (DMOG) induced hypoxia-inducible factor 1-alpha (HIF1α) upregulation, which enhanced IL-11 expression in NSCLC cells. Conclusions: Taken together, our results indicate that IL-11 is an oncogene in NSCLC, and elucidating the mechanism behind it may provide insights for NSCLC treatment.


Tumor Biology ◽  
2014 ◽  
Vol 35 (10) ◽  
pp. 9777-9785 ◽  
Author(s):  
Ji Zhou ◽  
Hui Bi ◽  
Ping Zhan ◽  
Cunjie Chang ◽  
Chunhua Xu ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document