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Updated: Jan 18, 2026
Patient Derived Cell Culture and Isolation of CD133+ Putative Cancer Stem Cells from Melanoma
Published on: March 13, 2013
Downregulation of KCTD12 contributes to melanoma stemness by modulating CD271
Weiyu Shen1, Yumei Li1, Bifei Li1
1Cancer Metastasis Alert and Prevention Center, College of Chemistry and Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou 350108, China.
Objective:
Cancer metastasis remains the primary cause of cancer-related death worldwide. In a previous study, we found that levels of BTB/POZ domain-containing protein KCTD12 are lower in metastatic melanoma cells than in parental melanoma cells. The purpose of this study was to identify the roles of KCTD12 in cancer metastasis.
Methods:
The Cancer Genome Atlas (TCGA) datasets were used to evaluate the relationship between KCTD12 and skin cutaneous melanoma (SKCM) prognosis. The effects of endogenous KCTD12 on biological behaviors were examined using the MTT assay. The impacts of KCTD12 on melanoma stemness were explored using spheroid formation assay. KCTD12 knockout A375 cells were generated to confirm the inhibitory effect of KCTD12 on CD271, and a mouse metastatic model was used to determine the impact of KCTD12 on melanoma metastasis in vivo.
Results:
KCTD12 levels were lower in lung metastatic cells than in paired parental melanoma cells, and low KCTD12 expression indicated a poor prognosis in SKCM. Cancer metastasis-related capacities were higher in lung metastatic cells than in parental melanoma cells. Moreover, KCTD12 knockdown enhanced tumor growth and metastasis both in vitro and in vivo. Mechanistically, the interaction between KCTD12 and CD271 might be responsible for the stemness transformation after KCTD12 knockdown.
Conclusions:
This study identifies for the first time the role of the interaction between KCTD12 and CD271 in inducing melanoma cell stemness transformation. Moreover, KCTD12 repression enhances melanoma cell growth, adhesion, migration and invasion.
Insights
BTB/POZ domain-containing protein KCTD12 is lower in metastatic melanoma. KCTD12 repression enhances melanoma growth and metastasis by affecting stemness and CD271 interaction.
Area of Science:
- Oncology
- Cancer Biology
- Melanoma Research
Background:
- Cancer metastasis is a leading cause of cancer mortality globally.
- Previous research indicated lower levels of KCTD12 in metastatic melanoma cells.
- Understanding KCTD12's role is crucial for developing anti-metastasis strategies.
Purpose of the Study:
- To investigate the function of KCTD12 in melanoma metastasis.
- To elucidate the molecular mechanisms underlying KCTD12's involvement in cancer progression.
Main Methods:
- Analysis of TCGA datasets for KCTD12 and SKCM prognosis.
- In vitro assays (MTT, spheroid formation) to assess biological behaviors and stemness.
- In vivo mouse model and KCTD12 knockout cells to confirm metastasis and CD271 interaction.
Main Results:
- Low KCTD12 expression correlates with poor SKCM prognosis.
- KCTD12 knockdown increased melanoma cell growth, metastasis, adhesion, migration, and invasion.
- KCTD12 knockdown enhanced stemness, potentially via interaction with CD271.
Conclusions:
- KCTD12 plays a significant inhibitory role in melanoma metastasis.
- The KCTD12-CD271 interaction is critical for melanoma stemness transformation.
- KCTD12 repression promotes melanoma progression, highlighting its therapeutic potential.
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