Table 1.

Selected upregulated sialyltransferase subtypes and their implications in cancer metastasis.

Sialyltransferase	Link to Cancer Progression and Metastasis	Reference(s)
A.  ST3Gal Family
ST3Gal-I	Upregulated in many cancer types (breast, ovarian, non-melanoma, and bladder cancer); overexpression promoted mammary tumorigenesis in mice and ovarian cancer cell migration, invasion (by inducing EMT), and conferred paclitaxel resistance	[32,33,34,35,44,51]
ST3Gal-II	Elevated ST3Gal-II mRNA levels observed in oral cancer with potential role in disease progression and metastasis	[50]
ST3Gal-III	Upregulated in different cancers (cervical, ovarian, oral, and breast); increased sLex expression, E-selectin adhesion, migration, and metastatic potential in pancreatic and breast adenocarcinoma cells; induced protein expression of metastasis-related proteins such as β1 integrin and matrix metalloproteinases (MMP-2 and MMP-9)	[36,37,38,39,45,46,47,50]
ST3Gal-IV	High ST3Gal-IV expression levels were observed in gastric and hepatic cancer cells; increased sLex expression, E-selectin adhesion, migration, and metastatic potential in ST3Gal-IV-overexpressing pancreatic cancer cells; induced sLex expression and c-Met activation in gastric carcinoma cells	[36,37,38,40,48,49]
ST3Gal-VI	Upregulation was associated with inferior survival in multiple myeloma; knockdown reduced cell adhesion and migration both in vitro and in vivo; increased expression levels promoted cell proliferation, migration, and invasion in liver cancer cells	[41,42]
B.  ST6Gal Family
ST6Gal-I	Upregulated in various carcinomas (colon, hepatic, non-melanoma, cervical, breast, ovarian, pancreatic, gastric, and non-small cell lung cancer) which correlated with distant metastasis, poor survival, EMT induction, and tumor invasion; known to induce β1 integrin-FAK mediated cell motility and migration as well as mediate invasiveness and tumorigenicity via the Notch1/Hes1/MMPs pathway; promoted chemoresistance and/or immune escape in several carcinoma cells	[13,43,44,45,49,52,53,54,63,64,65,66,67,68,69,70,71,72,73,74,75,76]
ST6Gal-II	High expression levels were associated with focal adhesion and metastasis pathways; downregulation inhibited levels of ICAM-1, VCAM-1, CD24, MMP2, MMP9, and CXCR4	[79]
C.  ST6GalNAc Family
ST6GalNAc-I	Overexpressed in breast and gastric cancer; responsible for the expression of sialyl-Tn (sTn) antigen which highly correlated with chemotherapeutic resistance and cancer metastasis	[81,83,84,85,86,87]
ST6GalNAc-II	Linked to the synthesis of sialyl-Tn (sTn) antigen associated with cancer aggressiveness; mediated follicular thyroid cancer cell invasion by regulating PI3K/Akt/NF-κB signaling pathway	[83,88]
ST6GalNac-V	Promoted breast cancer metastasis to the brain	[80]
D.  ST8Sia Family
ST8Sia-I	Upregulated in colon and breast cancer; mediated tumor growth and metastasis in triple-negative breast cancer; inhibition of ST8Sia-I led to suppression of FAK/Akt/mTOR and Wnt/β-catenin signaling pathways	[89,90,91,92,93]
ST8Sia-II	The highly invasive and migratory capabilities of glioma cells were found to be dependent on polySia expression	[96,97]