Expression of CD147 and Lewis y antigen in ovarian cancer and their relationship to drug resistance

Gao, Jian; Hu, Zhenhua; Liu, Juanjuan; Liu, Dawo; Wang, Yanyan; Cai, Mingbo; Zhang, Danye; Tan, Mingzi; Lin, Bei

doi:10.1007/s12032-014-0920-9

Cited by 28 publications

(28 citation statements)

References 34 publications

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“…As a result, exploring the mechanism of drug resistance has become an important direction of current research. Lewis y antigen was reported to be positively correlated with CD147 in resistance to chemotherapeutic drugs in ovarian cancer by using immunohistochemical assays, and the results indicated that CD147 and Lewis y antigen expression were all independent risk factors for chemoresistance in ovarian cancer at the pathological stage [9]. Additionally, a study demonstrated the co-localization of annexin II and Lewis y antigen through the double-labeling immunofluorescence experiments, and that annexin II contained Lewis y antigen [10].…”

Section: Discussionmentioning

confidence: 92%

Alpha1,2-fucosyl transferase gene, the key enzyme of Lewis y synthesis, promotes Taxol resistance of ovarian carcinoma through apoptosis-related proteins

Li¹,

Sha²,

Qin³

et al. 2018

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We aimed to investigate the role of FUT1 gene in Taxol resistance and to explore its mechanism in epithelial ovarian cancer. Three ovarian cancer cell lines, ES-2, SK-OV-3 and OVCAR-3 were selected from epithelial ovarian cancer in this experiment. Western blot was used to validate the protein expression level of FUT1 and the apoptosis proteins. The expression level of the corresponding carrier was validated by RT-PCR. Transfection and isolation of stable transfectants were carried out to establish the cell line models. The different concentrations of Taxol on the inhibition of cell growth rate was measured by MTT, in which Taxol resistance profiling in ovarian cancer cells was determined by IC50 data. Flow cytometry was conducted to compare cell apoptosis ability. Caspase-3 activity and the apoptosis proteins were measured by colorimetry and western blot, respectively, to further compare the cell apoptosis ability in different groups. To demonstrate the inhibition of miR-FUT1 combined with Taxol therapy against ovarian cancer, xenograft assay was carried out for the in vivo effect. The western blot results indicate that FUT1 is expressed in all of the ovarian cancer cells with different expression level: ES-2 > SK-OV-3 > OVCAR-3. Besides, FUT1 siRNA was used in the maximum expression of FUT1 cell line ES-2, or over-expression plasmid was used in the minimum expression of FUT1 cell line OVCAR-3, to establish stable expression cell lines. After the treatment with Taxol, the inhibition rate of Taxol was obviously decreased with the established cell model above, and the IC50 level was significantly increased in the FUT1 over-expression + Taxol group (p Keywords: FUT1, Lewis y, Taxol resistance, ovarian cancer, apoptosis.

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Section: Discussionmentioning

confidence: 92%

Alpha1,2-fucosyl transferase gene, the key enzyme of Lewis y synthesis, promotes Taxol resistance of ovarian carcinoma through apoptosis-related proteins

Li¹,

Sha²,

Qin³

et al. 2018

neo

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“…It mainly participates in cell-cell or cell-matrix interactions, stimulating adjacent fibroblasts to secrete a large numbers of matrix metalloproteinases (MMPs) and affects the invasion and metastasis of tumors. In addition, CD147 can suppress apoptosis and anoikis [21, 38], promote neovascularization, enhance resistance to several chemotherapeutic drugs [3, 17], promote the use of glycolysis in energy metabolism, and protect tumor cells from death [14, 20]. Another study has shown that CD147 is associated with autophagy [12], but did not identify a mechanism.…”

Section: Discussionmentioning

confidence: 99%

“…Expressed at high level, CD147 can promote the invasion and metastasis of tumor cells [35, 39], inhibit cell apoptosis and anoikis [21, 23], contribute to neo-vascularization and enhance resistance to several chemotherapeutic drugs [3, 17]. Gou X et al reported that CD147 involvement in the development of liver cancer is related to restrain autophagic cell death in liver cancer [12].…”

Section: Introductionmentioning

confidence: 99%

“…We found that the ovarian cancer cell lines with high levels of Lewis y antigen expression showed accelerated proliferation, reduced apoptosis, shortened cell cycle, and enhanced in vivo oncogenicity; after blockage with a monoclonal antibody against Lewis y antigen, the malignant behaviors of the cells were significantly weakened [11, 25, 40]. Furthermore, our preliminary work also indicated that Lewis y antigen is a part of the CD147 protein structure and that increased expression of Lewis y antigen strengthened the ability of CD147 to promote the adhesion and invasion of ovarian cancer cells [10]. …”

Section: Introductionmentioning

confidence: 99%

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The fucosylated CD147 enhances the autophagy in epithelial ovarian cancer cells

Cai

Deng

et al. 2016

Oncotarget

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Autophagy is modulated by multiple factors including CD147, but little is know about the effects and mechanism by which the modification of CD147 by Lewis y antigen regulates autophagy of ovarian cancer cell. Here, we reported that Lewis y antigen can promote basic autophagy activity and restrain autophagic cell death in ovarian cancer cells. Furthermore, human whole genome expression profile microarrays and massage pathway analysis revealed that during early stages of autophagy in ovarian cancer cells with highly expressing Lewis y antigen, PI3K/Akt-mTOR activity was reduced, in contrast, the PI3K/Akt-mTOR signaling pathway was activated as the length of amino acid deprivation increased, which inhibited eIF4G2 expression, further decreased the transcription of autophagy-related genes, suppressed autophagic cell death. we also elaborated that co-regulates protein degradation in cells via the ubiquitin-proteasome system and the autophagy-lysosome pathway. These findings suggested that the modification of CD147 by Lewis y antigen enhanced the survival ability by promoting basic autophagy activity and restraining autophagic cell death in ovarian cancer, thus playing an important role in ovarian cancer malignant progression.

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“…Известно, что EMMPRIN, выделенный из опухолевых клеток, паракринным способом стимулирует продукцию матричных металлопротеиназ соседними фибробластами [97]. Кроме того, он также стимулирует экспрессию фактора роста эндотелия сосудов и гиалуроновой кислоты, что приводит к ангиогенезу и множественной лекарственной устойчивости, которая, возможно, развивается путём активации фосфатидилинозитол-3-гидроксикиназы (PI3K) и митоген-активированных протеинкиназ (MAPK) [98]. Повышенная секреция EMMPRIN с сопутствующим увеличением секреции MMР-9 может обеспечивать более высокий метастатический потенциал, поскольку повышенная экспрессия этих двух белков выявлена при раке предстательной железы и плоскоклеточной карциноме шейки матки и является плохим прогностическим показателем для данных пациентов [99].…”

Section: роль тетраспанинов и протеаз экзосом в прогрессии злокачествunclassified

The role of exosomal tetraspanins and proteases in tumor progression

et al. 2018

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Major (CD9, CD63, CD81) and others (CD82, CD151, Tspan8) tetraspanins are widely represented in exosomes, where they interact with various proteins and form functional tetraspanin complexes. Tetraspanin complexes include proteases. Tetraspanin-associated exosomal proteases (ADAM proteases, MMPs, EMMPRIN) play an important role in the processes of cell motility, migration, invasion and formation of metastases. Also, a significant contribution to tumor progression is made by proteases that are not associated with tetraspanins. They destabilize intercellular contacts, promote migration and invasion of tumor cells, participate in the regulation of the expression IGF-I, VEGF and transcription factors activation/deactivation. The role of other proteases of exosomes in the processes of tumor progression is being clarified.

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Expression of CD147 and Lewis y antigen in ovarian cancer and their relationship to drug resistance

Cited by 28 publications

References 34 publications

Alpha1,2-fucosyl transferase gene, the key enzyme of Lewis y synthesis, promotes Taxol resistance of ovarian carcinoma through apoptosis-related proteins

Alpha1,2-fucosyl transferase gene, the key enzyme of Lewis y synthesis, promotes Taxol resistance of ovarian carcinoma through apoptosis-related proteins

The fucosylated CD147 enhances the autophagy in epithelial ovarian cancer cells

The role of exosomal tetraspanins and proteases in tumor progression

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