CD147-CD98hc Complex Contributes to Poor Prognosis of Non-Small Cell Lung Cancer Patients Through Promoting Cell Proliferation Via the PI3K/Akt Signaling Pathway

Fei, Fei; Li, Xiaofei; Xu, Li; Li, Deyang; Zhang, Zhipei; Guo, Xu; Yang, Hushan; Chen, Zhi‐Nan; Xing, Jinliang

doi:10.1245/s10434-014-3816-1

Cited by 43 publications

(40 citation statements)

References 33 publications

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“…SLC3A2 is upregulated in human osteosarcoma and promotes tumor growth via the PI3K/Akt signaling pathway [25]. In addition, the PI3K/Akt signaling pathway is also involved in CD147-SLC3A2-induced cell proliferation and the poor prognosis of non-small-cell lung cancer patients [26]. The PI3K/Akt signaling pathway is a key regulator of proliferation, apoptosis, and metastasis, and it constitutes a target for the treatment of ovarian cancer [27-29].…”

Section: Discussionmentioning

confidence: 99%

ZEB1 Promotes Chemoresistance to Cisplatin in Ovarian Cancer Cells by Suppressing SLC3A2

et al. 2018

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Ovarian cancer is one of the deadliest gynecological malignancies in women. Chemoresistance has been a major obstacle for ovarian cancer treatment. Zinc finger E-box-binding homeobox 1 (ZEB1) is an important regulator of tumor development in various types of cancer. Abnormal expression of SLC3A2 (CD98hc), a type 2 transmembrane cell surface molecule, has been described in several cancers. This study was designed to investigate the role of ZEB1 and SLC3A2 in the chemoresistance to cisplatin in ovarian cancer cells. We found that ZEB1 was increased in cisplatin-resistant SKOV3/DPP cells. Downregulation of ZEB1 significantly decreased cell viability in response to cisplatin, increased cisplatin-induced apoptosis, and decreased migration and invasion in the presence of cisplatin. In addition, downregulation of ZEB1 decreased the volume and weight of implanted tumors. SLC3A2 was decreased in cisplatin-resistant SKOV3/DPP cells. Upregulation of SLC3A2 significantly decreased cell viability in response to cisplatin, increased cisplatin-induced apoptosis, and decreased migration and invasion in the presence of cisplatin. Moreover, upregulation of SLC3A2 decreased the volume and weight of implanted tumors. Downregulation of ZEB1 resulted in a significant increase of SLC3A2 expression. Moreover, downregulation of SLC3A2 significantly inhibited ZEB1 knockdown-mediated inhibition of cisplatin-resistance. ZEB1-mediated regulation of SLC3A2 was involved in the chemoresistance to cisplatin in ovarian cancer cells. Overall, we provide new insights into the mechanism of chemoresistance to cisplatin in ovarian cancer cells. ZEB1/SLC3A2 may be promising therapeutic targets for enhancement of the sensitivity of ovarian cancer cells to cisplatin-mediated chemotherapy.

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Section: Discussionmentioning

confidence: 99%

ZEB1 Promotes Chemoresistance to Cisplatin in Ovarian Cancer Cells by Suppressing SLC3A2

et al. 2018

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“…LMO4 can inhibit the expression of the fusion proteinengrailed-LMO4 while suppressing cell growth, and can induce the apoptosis of breast cancer cells, indicating that LMO4 contributes to oncogenesis by similar mechanisms, thus enhancing cell survival and proliferation (19). AKT/PI3K activation is involved in the carcinogenesis and tumor progression of various solid tumors, including NSCLC (20,21). Lu et al reported that the transcriptional coactivator LMO4 modulated the cytostatic effects of TGF-beta in epithelial cells, and associated with and regulated a prototype Smad target promoter (14).…”

Section: Discussionmentioning

confidence: 99%

LMO4 is a prognostic marker involved in cell migration and invasion in non-small-cell lung cancer

Wang

Guo

et al. 2016

J. Thorac. Dis.

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Background: The aims of this study were to analyze the association of LMO4 with non-small-cell lung cancer (NSCLC) survival rate, and to determine its functional role and signaling pathway in lung cancer. Methods: Immunohistochemistry (IHC) was used to detect the expression of LMO4 in NSCLC cell lines and tumor tissues. Migration and invasion ability was detected respectively by wound healing test and transwell test. Immunofluorescence and western blot were detected of AKT/PI3K pathway related genes MAPK, PI3K, AKT. Results: LMO4 has high expression level of NSCLC cell lines and tumor tissues, and correlated with a lower survival rate. LMO4 can regulate the migration and invasion of NSCLC cells through the AKT/PI3K pathway. Conclusions: LMO4 could serve as a promising biomarker and therapeutic target for NSCLC.

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“…Because CD147 activates PI3K/Akt signaling in many cell types [24,25], we hypothesized that CD147-activated Akt/mTOR pathway may promote the SREBP1c-mediated up-regulation of lipogenic enzymes. Western blot analysis showed that the phosphorylations of both Akt and mTOR were significantly decreased in cells with CD147 knockout or knockdown, while reversion of CD147 expression in knockout cells (SMMC-7721/CD147-R) restored the phosphorylation levels of both Akt and mTOR ( Figures 4A and S4A).…”

Section: Cd147 Silencing Significantly Decreased Lipid Contents In Hcmentioning

confidence: 99%

CD147 reprograms fatty acid metabolism in hepatocellular carcinoma cells through Akt/mTOR/SREBP1c and P38/PPARα pathways

Huang

et al. 2015

Journal of Hepatology

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CD147-CD98hc Complex Contributes to Poor Prognosis of Non-Small Cell Lung Cancer Patients Through Promoting Cell Proliferation Via the PI3K/Akt Signaling Pathway

Abstract: Our findings indicate that the CD147-CD98hc complex significantly contributes to poor prognosis of NSCLC patients through promoting cell proliferation via the PI3K/Akt pathway.

Cited by 43 publications

References 33 publications

ZEB1 Promotes Chemoresistance to Cisplatin in Ovarian Cancer Cells by Suppressing SLC3A2

ZEB1 Promotes Chemoresistance to Cisplatin in Ovarian Cancer Cells by Suppressing SLC3A2

LMO4 is a prognostic marker involved in cell migration and invasion in non-small-cell lung cancer

CD147 reprograms fatty acid metabolism in hepatocellular carcinoma cells through Akt/mTOR/SREBP1c and P38/PPARα pathways

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