ORCID Profile
0000-0001-6452-1778
Current Organisation
University of Macau
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Publisher: Royal Society of Chemistry (RSC)
Date: 2019
DOI: 10.1039/C9CC05245C
Abstract: A chiral amino acid functionalized probe, PTZ-D, could self-assemble into a chiral organogel displaying unprecedented chiroptical monitoring of ClO − with switchable CPL signals.
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814807.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814804.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814810.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814795.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814792.V1
Abstract: supp. figure legends S1-S7
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814789.V1
Abstract: All supplementary tables in one excel file
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814807
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814819
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814810
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814789
Abstract: All supplementary tables in one excel file
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814813
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814804
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 25-05-2023
DOI: 10.1158/0008-5472.CAN-22-3398
Abstract: BRCA1 deficiency generates an acidic microenvironment to promote cancer metastasis and immunotherapy resistance that can be reversed using a sialyltransferase inhibitor.
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814816
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814792
Abstract: supp. figure legends S1-S7
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.C.6769338
Abstract: Abstract Cancer metastasis is an extremely complex process affected by many factors. An acidic microenvironment can drive cancer cell migration toward blood vessels while also h ering immune cell activity. Here, we identified a mechanism mediated by sialyltransferases that induces an acidic tumor-permissive microenvironment (ATPME) in BRCA1-mutant and most BRCA1-low breast cancers. Hypersialylation mediated by ST8SIA4 perturbed the mammary epithelial bilayer structure and generated an ATPME and immunosuppressive microenvironment with increased PD-L1 and PD1 expressions. Mechanistically, BRCA1 deficiency increased expression of VEGFA and IL6 to activate TGFβ–ST8SIA4 signaling. High levels of ST8SIA4 led to accumulation of polysialic acid (PSA) on mammary epithelial membranes that facilitated escape of cancer cells from immunosurveillance, promoting metastasis and resistance to αPD1 treatment. The sialyltransferase inhibitor 3Fax-Peracetyl Neu5Ac neutralized the ATPME, sensitized cancers to immune checkpoint blockade by activating CD8 T cells, and inhibited tumor growth and metastasis. Together, these findings identify a potential therapeutic option for cancers with a high level of PSA. Significance: BRCA1 deficiency generates an acidic microenvironment to promote cancer metastasis and immunotherapy resistance that can be reversed using a sialyltransferase inhibitor. /
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814813.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.C.6769338.V1
Abstract: Abstract Cancer metastasis is an extremely complex process affected by many factors. An acidic microenvironment can drive cancer cell migration toward blood vessels while also h ering immune cell activity. Here, we identified a mechanism mediated by sialyltransferases that induces an acidic tumor-permissive microenvironment (ATPME) in BRCA1-mutant and most BRCA1-low breast cancers. Hypersialylation mediated by ST8SIA4 perturbed the mammary epithelial bilayer structure and generated an ATPME and immunosuppressive microenvironment with increased PD-L1 and PD1 expressions. Mechanistically, BRCA1 deficiency increased expression of VEGFA and IL6 to activate TGFβ–ST8SIA4 signaling. High levels of ST8SIA4 led to accumulation of polysialic acid (PSA) on mammary epithelial membranes that facilitated escape of cancer cells from immunosurveillance, promoting metastasis and resistance to αPD1 treatment. The sialyltransferase inhibitor 3Fax-Peracetyl Neu5Ac neutralized the ATPME, sensitized cancers to immune checkpoint blockade by activating CD8 T cells, and inhibited tumor growth and metastasis. Together, these findings identify a potential therapeutic option for cancers with a high level of PSA. Significance: BRCA1 deficiency generates an acidic microenvironment to promote cancer metastasis and immunotherapy resistance that can be reversed using a sialyltransferase inhibitor. /
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814816.V1
Abstract: Original picture
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814795
Abstract: Original picture
Publisher: Elsevier BV
Date: 04-2023
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814819.V1
Abstract: Original picture
No related grants have been discovered for Xuanjun Zhang.