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Rei Mizuno1,2,3,4, Priya Chatterji1,2,3,4, Sarah Andres1,2,3,4

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The LIN28B-short isoform antagonizes the LIN28B-long isoform in colorectal cancer cells by preserving LET-7 expression. This suggests the short isoform may counteract the long isoform

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Area of Science:

  • Molecular biology
  • Cancer research
  • RNA biology

Background:

  • LIN28B protein has two isoforms: long and short.
  • The long isoform's role in cancer is known, but the short isoform's function is unclear.
  • Isoform expression differs in colorectal cancer versus normal tissue.

Purpose of the Study:

  • To investigate the distinct functions of LIN28B-long and -short isoforms in colorectal cancer.
  • To elucidate the mechanisms underlying their differential roles.
  • To explore their impact on cancer cell signaling and drug resistance.

Main Methods:

  • Generated colorectal cancer cells expressing no LIN28B, LIN28B-short, or LIN28B-long.
  • Analyzed LET-7 expression, RAS/ERK signaling, and drug resistance.
  • Investigated pre-let-7 binding and maturation inhibition.

Main Results:

  • LIN28B-long suppressed LET-7 and activated RAS/ERK signaling.
  • LIN28B-long increased resistance to 5-fluorouracil and cisplatin via ERCC1 upregulation in a LET-7-dependent manner.
  • LIN28B-short bound pre-let-7 without inhibiting maturation and competed with the long isoform.
  • Coexpression of the short isoform rescued phenotypes induced by the long isoform.

Conclusions:

  • LIN28B-short antagonizes LIN28B-long by preserving LET-7 maturation.
  • The short isoform may counterbalance the long isoform in normal colonic epithelium.
  • Downregulation of the short isoform during carcinogenesis may promote tumor growth via the long isoform's effects.