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Lnc-FAM84B-4 acts as an oncogenic lncRNA by interacting with protein hnRNPK to restrain MAPK phosphatases-DUSP1

Wen Peng1, Chuan Zhang1, Jianing Peng2

  • 1The First School of Clinical Medicine, Nanjing Medical University, PR China, Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, PR China.

Cancer Letters
|September 1, 2020
PubMed

Insights

Long non-coding RNA FAM84B (lnc-FAM84B-4) promotes colorectal cancer (CRC) by inhibiting DUSP1 expression. This lnc-FAM84B-4-hnRNPK-DUSP1 axis offers a potential therapeutic target for CRC treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • The mitogen-activated protein kinase (MAPK) pathway is crucial in cancer development.
  • Dual-specificity MAPK phosphatases (MKPs/DUSPs) regulate MAPK activity but their role in colorectal cancer (CRC) is unclear.

Purpose of the Study:

  • To investigate the roles of lnc-FAM84B-4 and DUSP1 in the MAPK pathway and CRC.
  • To elucidate the regulatory mechanism of lnc-FAM84B-4 in CRC.

Main Methods:

  • Re-mining CRC microarray data to identify upregulated lnc-FAM84B-4.
  • In vitro and in vivo functional assays.
  • RNA-Seq, RNA pull-down, and RIP assays to determine molecular mechanisms.

Main Results:

  • lnc-FAM84B-4 was upregulated in CRC and restrains DUSP1 expression, thereby regulating the MAPK pathway.
  • hnRNPK was identified as a binding partner of lnc-FAM84B-4, mediating DUSP1 expression.
  • The lnc-FAM84B-4-hnRNPK-DUSP1 axis plays a significant role in CRC development.

Conclusions:

  • lnc-FAM84B-4 promotes CRC by inhibiting DUSP1 expression via the hnRNPK-dependent mechanism.
  • The identified axis represents a potential therapeutic target for colorectal cancer treatment.
Keywords:
Colorectal cancerDUSPsLncRNAMAPKhnRNPK

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