Dual effects of an anti-CD147 antibody for Esophageal cancer therapy

Wang, Miao; Zhang, Shuai; Sun, Qian; Wang, Yu; Shang, Runze; Zhu, Yumeng; Yao, Hui; Li, Yu

doi:10.1080/15384047.2019.1647052

Cited by 15 publications

(17 citation statements)

References 30 publications

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“…Zhang et al [63] provided evidence that chimeric antigen receptor T cells induced by doxycycline targeting BSG could be used in the treatment of liver cancer. Another study also found that doxycycline inhibited the proliferation of gallbladder cancer cells by downregulating the expression levels of BSG and induced an early apoptosis response in cancer cells [64]. In addition, Wang et al [65] found that metuzumab could inhibit metastasis of esophageal cancer via blocking the function of BSG.…”

Section: Discussionmentioning

confidence: 95%

Immunohistochemical basigin expression level in thyroid cancer tissues

et al. 2020

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Background: Thyroid cancer (TC) is the most common endocrine malignancy; basigin (also known as BSG) plays a crucial role in tumor cell invasion, metastasis, and angiogenesis. This study was designed to identify the change of BSG expression in TC and its possible potential mechanism. Methods: The BSG expression levels in TC were demonstrated using data collected from in-house immunohistochemical (IHC), RNA-sequencing (RNA-seq), microarrays, and literatures. Integrated analysis was performed to determined BSG expression levels in TC comprehensively. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed with the integration of BSG co-expressed genes and differentially expressed genes (DEGs) in TC tissues to explore the potential mechanisms of BSG in TC. Results: The protein expression level of BSG was significantly higher in TC cases based on the IHC experiments. In addition, the combined SMD for BSG expression was 0.39 (p < 0.0001), the diagnostic odds ratio was 3.69, and the AUC of the sROC curve was 0.6986 using 1182 TC cases and 437 non-cancerous cases from 17 independent datasets. Furthermore, BSG co-expressed genes tended to be enriched in gene terms of the extracellular matrix (ECM), cell adhesion, and cell-cell interactions. The expression levels of nine hub BSG co-expressed genes were markedly upregulated in TC cases. Conclusion: BSG expression levels were closely correlated with the progression of TC and may affect the signals of the ECM, cell adhesion, and cell-cell interactions.

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Section: Discussionmentioning

confidence: 95%

Immunohistochemical basigin expression level in thyroid cancer tissues

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Zhang et al [63] provided evidence that chimeric antigen receptor T cells induced by doxycycline targeting BSG can be used in the treatment of liver cancer. Another study also found that doxycycline inhibited the proliferation of gallbladder cancer cells by down-regulating the expression levels of BSG and induced an early apoptosis response in cancer cells [64]. In addition, Wang et al [65] found that Metuzumab could inhibit metastasis of esophageal cancer via blocking the function of BSG.…”

Section: Discussionmentioning

confidence: 95%

Immunohistochemical Basigin Expression Level in Thyroid Cancer Tissues

Guo

Tang

Pang

et al. 2020

Preprint

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Background: Thyroid cancer (TC) is the most common endocrine malignancy, Basigin (also known as BSG) plays a crucial role in tumor cell invasion, metastasis, and angiogenesis. This study was designed to identify the change of BSG expression in TC and its possible potential mechanism. Methods: The BSG expression levels in TC were demonstrated using data collected from in-house immunohistochemical (IHC), RNA-sequencing (RNA-seq), microarrays and literatures. Integrated analysis was performed to determined BSG expression levels in TC comprehensively. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed with the integration of BSG co-expressed genes and differentially expressed genes (DEGs) in TC tissues to explore the potential mechanisms of BSG in TC. Results: The protein expression level of BSG was significantly higher in TC cases based on the IHC experiments. In addition, the combined SMD for BSG expression was 0.39 (p<0.0001), the diagnostic odds ratio was 3.69, and the AUC of the sROC curve was 0.6986 using 1182 TC cases and 437 non-cancerous cases from 17 independent datasets. Furthermore, BSG co-expressed genes tended to be enriched in gene terms of the extracellular matrix (ECM), cell adhesion, and cell-cell interactions. The expression levels of nine hub BSG co-expressed genes were markedly up-regulated in TC cases. Conclusion: BSG expression levels were closely correlated with the progression of TC and may affect the signals of the ECM, cell adhesion, and cell-cell interactions.

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“…These results, although preliminary and confirmed only in a small number of patients, suggest a possible contribution of CD147/basigin upregulation in BRAFi/MEKi resistance. Interestingly, several inhibitors [ 72 ] or an antibody [ 73 ] targeting CD147/basigin have been suggested as potential therapeutic agents.…”

Section: Discussionmentioning

confidence: 99%

Melanoma Cell Resistance to Vemurafenib Modifies Inter-Cellular Communication Signals

et al. 2021

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The therapeutic success of BRAF inhibitors (BRAFi) and MEK inhibitors (MEKi) in BRAF-mutant melanoma is limited by the emergence of drug resistance, and several lines of evidence suggest that changes in the tumor microenvironment can play a pivotal role in acquired resistance. The present study focused on secretome profiling of melanoma cells sensitive or resistant to the BRAFi vemurafenib. Proteomic and cytokine/chemokine secretion analyses were performed in order to better understand the interplay between vemurafenib-resistant melanoma cells and the tumor microenvironment. We found that vemurafenib-resistant melanoma cells can influence dendritic cell (DC) maturation by modulating their activation and cytokine production. In particular, human DCs exposed to conditioned medium (CM) from vemurafenib-resistant melanoma cells produced higher levels of pro-inflammatory cytokines—that potentially facilitate melanoma growth—than DCs exposed to CM derived from parental drug-sensitive cells. Bioinformatic analysis performed on proteins identified by mass spectrometry in the culture medium from vemurafenib-sensitive and vemurafenib-resistant melanoma cells suggests a possible involvement of the proteasome pathway. Moreover, our data confirm that BRAFi-resistant cells display a more aggressive phenotype compared to parental ones, with a significantly increased production of interferon-γ, interleukin-8, vascular-endothelial growth factor, CD147/basigin, and metalloproteinase 2 (MMP-2). Plasma levels of CD147/basigin and MMP-2 were also measured before the start of therapy and at disease progression in a small group of melanoma patients treated with vemurafenib or vemurafenib plus cobimetinib. A significant increment in CD147/basigin and MMP-2 was observed in all patients at the time of treatment failure, strengthening the hypothesis that CD147/basigin might play a role in BRAFi resistance.

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Dual effects of an anti-CD147 antibody for Esophageal cancer therapy

Cited by 15 publications

References 30 publications

Immunohistochemical basigin expression level in thyroid cancer tissues

Immunohistochemical basigin expression level in thyroid cancer tissues

Immunohistochemical Basigin Expression Level in Thyroid Cancer Tissues

Melanoma Cell Resistance to Vemurafenib Modifies Inter-Cellular Communication Signals

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