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Updated: Jul 4, 2026

Isolation of Myoepithelial Cells from Adult Murine Lacrimal and Submandibular Glands

Isolation of Myoepithelial Cells from Adult Murine Lacrimal and Submandibular Glands

Published on: June 11, 2019

MYC Is Functionally Required in Both Normal and Neoplastic Meibomian Glands.

Isabella Boyack¹, Autumn Berlied¹, Su-Chan Lee²

¹Department of Comparative Pathobiology, Cummings School of Veterinary Medicine, Tufts University, North Grafton, Massachusetts.

The American Journal of Pathology

|July 2, 2026

Summary

MYC is crucial for Meibomian gland (MG) function and ocular adnexal sebaceous carcinoma (SebCA) growth. Inhibiting MYC significantly impairs MG proliferation and SebCA viability, highlighting MYC as a potential therapeutic target.

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Area of Science:

Ophthalmology
Oncology
Molecular Biology

Background:

The Meibomian gland (MG) is clinically important, but its proliferation and differentiation mechanisms are poorly understood.
Ocular adnexal sebaceous carcinoma (SebCA), a rare malignancy, often originates from the MG and is characterized by high MYC expression.

Purpose of the Study:

To investigate the dependence of the Meibomian gland on MYC.
To assess the therapeutic potential of MYC inhibition in SebCA.

Main Methods:

MYC-modulated murine MGs were analyzed using histopathology, morphometry, immunohistochemistry, and qPCR.
In vitro assays evaluated cell viability, differentiation, proliferation, and clonogenic potential.
MYC expression and concentration were quantified using ELISA and qPCR.

Main Results:

MYC inhibition in murine MGs led to reduced cytoplasmic volume, diminished proliferation, increased apoptosis, and altered lipid droplet formation.
MYC inhibition significantly impaired SebCA viability and clonogenicity, with reduced proliferation observed.
MYCMI6 demonstrated the most effective suppression of MYC transcriptional targets.

Conclusions:

MYC plays a critical role in Meibomian gland proliferation and differentiation.
MYC dysregulation is implicated in the oncogenic potential of SebCA.
Targeting MYC stability, transcriptional activity, or the MYC:MAX heterodimer may offer therapeutic strategies for MG disorders and SebCA.