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  1. Home
  2. Downregulation Of Rnf128 Inhibits The Proliferation, Migration, Invasion And Emt Of Colorectal Cancer Cells.
  1. Home
  2. Downregulation Of Rnf128 Inhibits The Proliferation, Migration, Invasion And Emt Of Colorectal Cancer Cells.

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Downregulation of RNF128 Inhibits the Proliferation, Migration, Invasion and EMT of Colorectal Cancer Cells.

Meng Wang1,2, Jian Ding2, Aihong Zhao1

  • 1The First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.

Biochemical Genetics
|August 15, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Ring finger protein 128 (RNF128) is elevated in colorectal cancer. Inhibiting RNF128 suppressed tumor growth, migration, and invasion, suggesting RNF128 as a potential therapeutic target for colorectal cancer.

Keywords:
Colorectal cancerEMTInvasionProliferationRNF128

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Colorectal cancer (CRC) is a leading cause of cancer incidence and mortality globally.
  • Understanding CRC's molecular drivers is crucial for improving patient outcomes.
  • The role of Ring finger protein 128 (RNF128) in CRC remains uncharacterized, despite its varied roles in other cancers.

Purpose of the Study:

  • To investigate the expression and function of RNF128 in colorectal cancer.
  • To determine if RNF128 plays a role in CRC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).

Main Methods:

  • Differential expression analysis of RNF128 mRNA and protein in 30 CRC tissues versus adjacent normal tissues using RT-qPCR, Western blot, and immunohistochemistry.
  • In vitro functional assays in CRC cell lines (SW1116, SW480) involving RNF128 knockdown via siRNA.
  • Assessment of cell proliferation (CCK-8, colony formation), migration (wound-healing), invasion (Transwell), and EMT markers (Western blot, immunofluorescence).
  • Main Results:

    • RNF128 mRNA and protein levels were significantly upregulated in colorectal cancer tissues compared to peritumoral tissues.
    • siRNA-mediated knockdown of RNF128 markedly inhibited proliferation, growth, migration, and invasion of CRC cell lines.
    • RNF128 inhibition also suppressed the epithelial-mesenchymal transition (EMT) process in CRC cells.

    Conclusions:

    • RNF128 is overexpressed in colorectal cancer and promotes tumor progression.
    • Targeting RNF128 demonstrates therapeutic potential for colorectal cancer treatment.
    • RNF128 represents a promising molecular target for managing colorectal cancer.