KCTD17

Last update 08 May 2025

Basic Info

Synonyms

BTB/POZ domain-containing protein KCTD17, FLJ12242, KCTD17

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Introduction

Substrate-adapter for CUL3-RING ubiquitin ligase complexes which mediates the ubiquitination and subsequent proteasomal degradation of TCHP, a protein involved in ciliogenesis down-regulation. Thereby, positively regulates ciliogenesis, playing a crucial role in the initial steps of axoneme extension (PubMed:25270598). May also play a role in endoplasmic reticulum calcium ion homeostasis (PubMed:25983243).

100 Clinical Results associated with KCTD17

100 Translational Medicine associated with KCTD17

0 Patents (Medical) associated with KCTD17

Literatures (Medical) associated with KCTD17

01 Jan 2025·Clinical and Molecular Hepatology

Identification of KCTD17 as a Ras stabilizer in hepatocellular carcinoma: Editorial on “KCTD17-mediated Ras stabilization promotes hepatocellular carcinoma progression”

Author: Leung, Rainbow Wing Hei ; Lee, Terence Kin Wah

01 Jan 2025·Clinical and Molecular Hepatology

Correspondence to editorial on “KCTD17-mediated Ras stabilization promotes hepatocellular carcinoma progression”

Article

Author: Kim, KyeongJin ; Lee, Sang Bae

01 Oct 2024·Clinical and Molecular Hepatology

KCTD17-mediated Ras stabilization promotes hepatocellular carcinoma progression

Article

Author: Jung, Young Hoon ; Lee, Yun Ji ; Gi, HyunJoon ; Kim, KyeongJin ; Pajvani, Utpal B ; Kim, Young Un ; Carrer, Michele ; Hong, Soon-Sun ; Lee, Sang Bae ; Oh, Ah-Reum ; Jung, Kyung Hee ; Ryu, Dongryeol ; Dao, Tam ; Jeong, Yelin ; Yu, Junjie

Background/Aims: Potassium channel tetramerization domain containing 17 (KCTD17) protein, an adaptor for the cullin3 (Cul3) ubiquitin ligase complex, has been implicated in various human diseases; however, its role in hepatocellular carcinoma (HCC) remains elusive. Here, we aimed to elucidate the clinical features of KCTD17, and investigate the mechanisms by which KCTD17 affects HCC progression.Methods: We analyzed transcriptomic data from patients with HCC. Hepatocyte-specific KCTD17 deficient mice were treated with diethylnitrosamine (DEN) to assess its effect on HCC progression. Additionally, we tested KCTD17-directed antisense oligonucleotides for their therapeutic potential in vivo.Results: Our investigation revealed the upregulation of KCTD17 expression in both tumors from patients with HCC and mouse models of HCC, in comparison to non-tumor controls. We identified the leucine zipper-like transcriptional regulator 1 (Lztr1) protein, a previously identified Ras destabilizer, as a substrate for KCTD17-Cul3 complex. KCTD17-mediated Lztr1 degradation led to Ras stabilization, resulting in increased proliferation, migration, and wound healing in liver cancer cells. Hepatocyte-specific KCTD17 deficient mice or liver cancer xenograft models were less susceptible to carcinogenesis or tumor growth. Similarly, treatment with KCTD17-directed antisense oligonucleotides (ASO) in a mouse model of HCC markedly lowered tumor volume as well as Ras protein levels, compared to those in control ASO-treated mice.Conclusions: KCTD17 induces the stabilization of Ras and downstream signaling pathways and HCC progression and may represent a novel therapeutic target for HCC.

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KCTD17

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