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Review
. 2020 Nov 4;28(11):2358-2366.
doi: 10.1016/j.ymthe.2020.08.021. Epub 2020 Sep 2.

xCT: A Critical Molecule That Links Cancer Metabolism to Redox Signaling

Jinyun Liu  1 , Xiaojun Xia  2 , Peng Huang  3
Affiliations
Review

"VSports app下载" xCT: A Critical Molecule That Links Cancer Metabolism to Redox Signaling

Jinyun Liu et al. Mol Ther. .

Abstract

System xc- cystine/glutamate antiporter, composed of a light-chain subunit (xCT, SLC7A11) and a heavy-chain subunit (CD98hc, SLC3A2), is mainly responsible for the cellular uptake of cystine in exchange for intracellular glutamate. In recent years, the xCT molecule has been found to play an important role in tumor growth, progression, metastasis, and multidrug resistance in various types of cancer VSports手机版. Interestingly, xCT also exhibits an essential function in regulating tumor-associated ferroptosis. Despite significant progress in targeting the system xc- transporter in cancer treatment, the underlying mechanisms still remain elusive. It is also unclear why solid tumors are more sensitive to xCT inhibitors such as sulfasalazine, as compared to hematological malignancies. This review mainly focuses on the role of xCT cystine/glutamate transporter in regard to tumor growth, chemoresistance, tumor-selective ferroptosis, and the mechanisms regulating xCT gene expression. The potential therapeutic implications of targeting the system xc- and its combination with chemotherapeutic agents or immunotherapy to suppress tumor growth and overcome drug resistance are also discussed. .

Keywords: ROS; ferroptosis; system x(c)(−); xCT. V体育安卓版.

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Figures

None
Graphical abstract
Figure 1
Figure 1
Cartoon Illustration of the xCT Regulators
Figure 2
Figure 2
Cartoon Illustration of xc− Transporter-Mediated Cystine/Cysteine Exchange between Stromal Cells and Cancer Cells Left: stroma cells provide cyst(e)ine to cancer cells through system alanine-serine-cysteine (ASC) or xc− transporters for cancer cell proliferation and drug resistance. Right: suppression of xCT expression by T cell-derived IFNγ or depletion of the extracellular cyst(e)ine by cyst(e)inase will block the stroma-cancer exchange and induce ROS/lipid ROS accumulation in cancer cells and subsequent apoptosis/ferroptosis.
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References

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