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Updated: Feb 17, 2026
Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
TAp73 inhibits cell invasion and migration by directly activating KAI1 expression in colorectal carcinoma
Woo-Kyun Bae1, Chang-Soo Hong1, Mi-Ra Park1
1Department of Hemato-Oncology, Chonnam National University Hwasun Hospital, Hwasun, South Korea.
Abstract:
p73 is a member of the p53 family of transcription factors and, like p53, plays a role as a tumor suppressor. p73 is involved in development, proliferation, apoptosis and metastasis. However, the precise molecular mechanisms underlying its function in inhibiting metastasis remain largely unknown. Here, we show that induction of TAp73 decreased invasion and migration activity of colorectal cancer cells, whereas knockdown of TAp73 led to increased invasion and migration activity. KAI1 was identified as a transcriptional target of TAp73 and its expression is indispensable for TAp73-mediated inhibition of cell invasion and migration. Furthermore, induction of TAp73 in colorectal cancer cells elevated KAI1 expression and decreased the frequency of hepatic metastasis in vivo. Whereas, the decreased invasion and migration activities caused by TAp73 induction were abrogated by knockdown of KAI1. Interestingly, TAp73 and KAI1 are overexpressed in primary colorectal cancers and a significant correlation between TAp73 and KAI1 expression was detected, but their expressions were significantly down-regulated in metastatic cancers. Taken together, our results support a novel role for TAp73 in controlling colorectal cancer cell invasion, migration and metastasis by regulating transcription of KAI1.
Insights
The tumor suppressor TAp73 inhibits colorectal cancer metastasis by upregulating KAI1 expression. This TAp73-KAI1 pathway is crucial for controlling cancer cell invasion and migration.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- p73, a p53 family member, functions as a tumor suppressor involved in development and apoptosis.
- The specific molecular mechanisms by which p73 inhibits cancer metastasis are not fully understood.
Purpose of the Study:
- To elucidate the role of TAp73 in regulating colorectal cancer cell invasion, migration, and metastasis.
- To identify the molecular targets and pathways involved in TAp73-mediated anti-metastatic effects.
Main Methods:
- Investigated the effects of TAp73 induction and knockdown on colorectal cancer cell invasion and migration in vitro.
- Identified KAI1 as a transcriptional target of TAp73 using molecular assays.
- Assessed the impact of TAp73 and KAI1 on hepatic metastasis in vivo.
- Analyzed TAp73 and KAI1 expression levels in primary and metastatic colorectal cancer tissues.
Main Results:
- TAp73 induction reduced colorectal cancer cell invasion and migration; TAp73 knockdown increased these activities.
- KAI1 expression was essential for TAp73's inhibitory effects on cell invasion and migration.
- TAp73 induction elevated KAI1 expression and decreased hepatic metastasis in vivo.
- TAp73 and KAI1 were overexpressed in primary colorectal cancers but downregulated in metastatic cancers, with a positive correlation between their expressions.
Conclusions:
- TAp73 plays a novel role in suppressing colorectal cancer metastasis.
- TAp73 exerts its anti-metastatic function by transcriptionally regulating KAI1.
- The TAp73-KAI1 axis represents a potential therapeutic target for inhibiting colorectal cancer progression.
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