KLF17

From WikiMD's Wellness Encyclopedia

KLF17 (Kruppel-like factor 17) is a protein that in humans is encoded by the KLF17 gene. It belongs to the Kruppel-like factor family, a group of transcription factors that play significant roles in cell differentiation, development, and metabolism. KLF17 has been identified as a critical regulator in various biological processes, including cell cycle regulation, apoptosis (programmed cell death), and epithelial-mesenchymal transition (EMT), a key event in cancer progression and metastasis.

Function[edit | edit source]

KLF17 functions as a transcriptional repressor and has been shown to inhibit the epithelial-mesenchymal transition, a process by which epithelial cells lose their cell polarity and cell-cell adhesion, and gain migratory and invasive properties. This transition is crucial for the development of many tissues and organs and is also implicated in the progression of various diseases, including cancer. By inhibiting EMT, KLF17 plays a role in suppressing tumor metastasis, particularly in breast cancer and lung cancer.

Gene[edit | edit source]

The KLF17 gene is located on chromosome 1, specifically at 1p34.1. It consists of several exons and encodes a protein that contains zinc finger domains, characteristic of the Kruppel-like factor family, which are essential for binding to DNA and regulating the expression of target genes.

Clinical Significance[edit | edit source]

Research has highlighted the potential role of KLF17 in cancer biology, especially in the context of its function as a metastasis suppressor. Loss of KLF17 expression has been associated with increased metastatic potential in breast cancer and lung cancer. Furthermore, KLF17 has been studied for its role in other diseases, including its potential involvement in the regulation of adipogenesis and its implications in obesity.

Potential Therapeutic Target[edit | edit source]

Given its role in inhibiting EMT and suppressing metastasis, KLF17 presents a potential therapeutic target for the treatment of metastatic cancers. Strategies to upregulate KLF17 expression or enhance its function could offer new avenues for cancer therapy, particularly for cancers that are prone to early metastasis.


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Contributors: Prab R. Tumpati, MD