SUSD6

Last update 23 Jan 2025

Basic Info

Synonyms

DRAGO, Drug-activated gene overexpressed protein, KIAA0247

+ [3]

Introduction

May play a role in growth-suppressive activity and cell death (PubMed:24652652). May be involved in the production of chemokine molecules in umbilical vein endothelial cells (HUVECs) cultured in THP1 monocyte LPS-induced medium (PubMed:20236627). Plays a role in preventing tumor onset (By similarity).

100 Clinical Results associated with SUSD6

100 Translational Medicine associated with SUSD6

0 Patents (Medical) associated with SUSD6

Literatures (Medical) associated with SUSD6

05 Oct 2023·Cancer discovery

A Cell-Surface MHC-I Inhibitory Axis Promotes Immune Evasion in Cancer.

Article

SUSD6, TMEM127, and WWP2 were identified as negative regulators of MHC-I in AML and solid tumors.

01 Aug 2023·CellQ1 · BIOLOGY

A membrane-associated MHC-I inhibitory axis for cancer immune evasion

Q1 · BIOLOGY

Article

Author: Zhang, Jiangyan ; Rona, Gergely ; Dahia, Patricia L M ; Cresswell, Peter ; Al-Santli, Wafa ; Guo, Qianjin ; Liu, Jia ; Pagano, Michele ; Cammer, Michael ; Aifantis, Iannis ; Lu, Qiao ; Wang, Jun ; Wang, Kun ; Lasry, Audrey ; Zhang, Hongbing ; Ciantra, Zoe ; Liu, Cheng ; Sengupta, Debrup ; Lai, Baoling ; Chen, Xufeng ; Zhou, Hua ; You, Jia ; Nadorp, Bettina ; Boukhris, Ahmad ; Sun, Zhengxi

Immune-checkpoint blockade has revolutionized cancer treatment, but some cancers, such as acute myeloid leukemia (AML), do not respond or develop resistance. A potential mode of resistance is immune evasion of T cell immunity involving aberrant major histocompatibility complex class I (MHC-I) antigen presentation (AP). To map such mechanisms of resistance, we identified key MHC-I regulators using specific peptide-MHC-I-guided CRISPR-Cas9 screens in AML. The top-ranked negative regulators were surface protein sushi domain containing 6 (SUSD6), transmembrane protein 127 (TMEM127), and the E3 ubiquitin ligase WWP2. SUSD6 is abundantly expressed in AML and multiple solid cancers, and its ablation enhanced MHC-I AP and reduced tumor growth in a CD8⁺ T cell-dependent manner. Mechanistically, SUSD6 forms a trimolecular complex with TMEM127 and MHC-I, which recruits WWP2 for MHC-I ubiquitination and lysosomal degradation. Together with the SUSD6/TMEM127/WWP2 gene signature, which negatively correlates with cancer survival, our findings define a membrane-associated MHC-I inhibitory axis as a potential therapeutic target for both leukemia and solid cancers.

01 Apr 2018·Cancer ScienceQ2 · MEDICINE

KIAA0247 inhibits growth, migration, invasion of non‐small‐cell lung cancer through regulating the Notch pathway

Q2 · MEDICINE

ArticleOA

Author: Wang, Qiongzi ; Qiu, Xueshan ; Ren, Hongjiu ; Zhang, Qingfu ; Su, Hongbo ; Jiang, Jun ; Xu, Yitong ; Wang, Chenglong ; Wudu, Muli ; Jiang, Lihong

Lung cancer remains the leading cause of cancer‐related death worldwide. Previous studies have shown that the novel KIAA0247 gene potentially targeted by the tumor suppressor p53 may inhibit the development of several cancers. However, the exact function of KIAA0247 in non‐small‐cell lung cancer (NSCLC) is unknown. The purpose of the present study was to clarify the role of KIAA0247 in NSCLC. KIAA0247 expression was evaluated in tumors and adjacent normal tissues of 197 NSCLC patients by immunohistochemistry and real‐time PCR and analyzed for association with clinicopathological parameters. Results indicated that KIAA0247 levels positively correlated with cell differentiation (P < .001) and patient survival (P < .0001) and negatively correlated with lymph node metastasis (P < .001) and advanced p‐TNM stage (P < .001). In cultured NSCLC cell lines, KIAA0247 overexpression inhibited cell migration, invasion, and proliferation and downregulated the expression of Jagged1, Notch1 intracellular domain (NICD), Snail, cyclin D1, RhoA, RhoC, and MMP9, while upregulating that of E‐cadherin and p21. The Notch inhibitor DAPT reduced the biological effects of KIAA0247 knockdown, suggesting that KIAA0247 decreased the carcinogenic activity of NSCLC cells through downregulation of Notch signaling. Our results indicate that KIAA0247 inhibits NSCLC progression by reducing the metastatic potential of cancer cells through downregulation of the Notch pathway, which may underlie the association of KIAA0247 expression with favorable clinicopathological characteristics of NSCLC patients. These findings suggest that KIAA0247 is a candidate prognostic biomarker and potential therapeutic target in NSCLC.

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