General Information of the Ferroptosis Regulator (ID: REG10408)
Regulator Name Sialic acid-binding Ig-like lectin 9 (SIGLEC9)
Synonyms
CDw329; Protein FOAP-9; CD_antigen=CD329
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Gene Name SIGLEC9
Gene ID 27180
Regulator Type Protein coding
Uniprot ID Q9Y336
Sequence
MLLLLLPLLWGRERAEGQTSKLLTMQSSVTVQEGLCVHVPCSFSYPSHGWIYPGPVVHGY
WFREGANTDQDAPVATNNPARAVWEETRDRFHLLGDPHTKNCTLSIRDARRSDAGRYFFR
MEKGSIKWNYKHHRLSVNVTALTHRPNILIPGTLESGCPQNLTCSVPWACEQGTPPMISW
IGTSVSPLDPSTTRSSVLTLIPQPQDHGTSLTCQVTFPGASVTTNKTVHLNVSYPPQNLT
MTVFQGDGTVSTVLGNGSSLSLPEGQSLRLVCAVDAVDSNPPARLSLSWRGLTLCPSQPS
NPGVLELPWVHLRDAAEFTCRAQNPLGSQQVYLNVSLQSKATSGVTQGVVGGAGATALVF
LSFCVIFVVVRSCRKKSARPAAGVGDTGIEDANAVRGSASQGPLTEPWAEDSPPDQPPPA
SARSSVGEGELQYASLSFQMVKPWDSRGQEATDTEYSEIKIHR

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Family SIGLEC (sialic acid binding Ig-like lectin) family
Function
Putative adhesion molecule that mediates sialic-acid dependent binding to cells. Preferentially binds to alpha-2,3- or alpha-2,6-linked sialic acid. The sialic acid recognition site may be masked by cis interactions with sialic acids on the same cell surface.

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HGNC ID
HGNC:10878
KEGG ID hsa:27180
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
SIGLEC9 can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
Browse Target
Browse Disease
Unspecific Target [Unspecific Target]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Responsed Disease Oesophageal cancer ICD-11: 2B70
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
TE-1 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1759
KYSE30 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1351
In Vivo Model
A total of 128 immune active female C57BL/6 mice (6 weeks old) were procured from SLAC Laboratory Animal Co., Ltd. (Shanghai, China). ESCC cells (TE-1 and KYSE-30) resuspended in PBS were mixed with Matrigel and subcutaneously injected into the mice (1 x 106 cells per mouse) at the right flank to induce subcutaneous tumors. When the tumor size reached around 150 mm3, the tumor site was locally exposed to irradiation (2 Gy/d for consecutive 4 d). For antibody injection, the mice were injected with IgG or Anti-SIGECE on day 1, 7, or 14 after the first irradiation exposure. After 28 d, the mice were euthanized via overdosed barbiturate (150 mg/kg). The subcutaneous tumors were collected for IHC. Another group of ESCC cells were injected into mice via tail vein (2 x 106 cells per mouse).

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Response regulation LINC01004 recruited Spi-1 proto-oncogene (SPI1) in nucleus of TAMs to induce transcriptional activation of SIGLEC9. SIGLEC9 interacted with mucin 1 (MUC1). MUC1 overexpression in esophageal squamous cell carcinoma (ESCC) induced M2 skewing of TAMs, enhanced radioresistance and immunosuppression, and promoted nuclear translocation of -catenin to suppress radiotherapy-induced ferroptosis of ESCC cells.
Oesophageal cancer [ICD-11: 2B70]
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Sialic acid-binding Ig-like lectin 9 (SIGLEC9) Protein coding
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
TE-1 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1759
KYSE30 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1351
In Vivo Model
A total of 128 immune active female C57BL/6 mice (6 weeks old) were procured from SLAC Laboratory Animal Co., Ltd. (Shanghai, China). ESCC cells (TE-1 and KYSE-30) resuspended in PBS were mixed with Matrigel and subcutaneously injected into the mice (1 x 106 cells per mouse) at the right flank to induce subcutaneous tumors. When the tumor size reached around 150 mm3, the tumor site was locally exposed to irradiation (2 Gy/d for consecutive 4 d). For antibody injection, the mice were injected with IgG or Anti-SIGECE on day 1, 7, or 14 after the first irradiation exposure. After 28 d, the mice were euthanized via overdosed barbiturate (150 mg/kg). The subcutaneous tumors were collected for IHC. Another group of ESCC cells were injected into mice via tail vein (2 x 106 cells per mouse).

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Response regulation LINC01004 recruited Spi-1 proto-oncogene (SPI1) in nucleus of TAMs to induce transcriptional activation of SIGLEC9. SIGLEC9 interacted with mucin 1 (MUC1). MUC1 overexpression in esophageal squamous cell carcinoma (ESCC) induced M2 skewing of TAMs, enhanced radioresistance and immunosuppression, and promoted nuclear translocation of -catenin to suppress radiotherapy-induced ferroptosis of ESCC cells.
References
Ref 1 LINC01004-SPI1 axis-activated SIGLEC9 in tumor-associated macrophages induces radioresistance and the formation of immunosuppressive tumor microenvironment in esophageal squamous cell carcinoma. Cancer Immunol Immunother. 2023 Jun;72(6):1835-1851. doi: 10.1007/s00262-022-03364-5. Epub 2023 Jan 23.