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Updated: May 15, 2026

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia

Published on: July 25, 2017

The ARF tumor-suppressor controls Drosha translation to prevent Ras-driven transformation.

M J Kuchenreuther¹, J D Weber²

¹1] BRIGHT Institute, Washington University School of Medicine, St Louis, MO, USA [2] Department of Internal Medicine, Division of Molecular Oncology, Washington University School of Medicine, St Louis, MO, USA.

|January 16, 2013

Summary

The ARF tumor suppressor regulates Drosha protein levels by controlling its mRNA translation. Loss of ARF leads to increased Drosha, promoting cell proliferation and Ras-driven transformation.

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Published on: March 9, 2012

Area of Science:

Molecular Biology
Oncology
RNA Biology

Background:

ARF is a tumor suppressor regulating ribosome biogenesis and sensing oncogenic stress.
DDX5, a microRNA (miRNA) microprocessor accessory, is a known ARF target.
Drosha, the catalytic core of the microprocessor complex, is essential for non-coding RNA maturation.

Purpose of the Study:

To identify novel molecular targets of ARF within the miRNA microprocessor complex.
To investigate the impact of ARF loss on Drosha expression and function.
To elucidate the role of Drosha in ARF-deficient cell proliferation and transformation.

Main Methods:

Analysis of Drosha protein and mRNA levels in Arf-deficient cells.
Investigation of Drosha mRNA translation and stability.
Assessment of miRNA and ribosomal RNA (rRNA) production.
Evaluation of cellular proliferation and oncogenic Ras(V12)-dependent transformation.

Main Results:

Loss of Arf significantly enhanced Drosha protein expression via increased mRNA translation, not transcription or stability.
Elevated Drosha levels altered a subset of miRNA expression and increased rRNA synthesis.
Increased Drosha was essential for maintaining proliferation and Ras(V12)-induced transformation in Arf-deficient cells.
Drosha knockdown inhibited Ras-dependent transformation in Arf-deficient cells.

Conclusions:

ARF suppresses tumor formation by regulating Drosha mRNA translation.
Aberrant Drosha expression contributes to uncontrolled cell proliferation and oncogenic transformation.
Targeting Drosha translation may offer therapeutic strategies against ARF-deficient cancers.