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Metaplasia is emerging as a key process in tumorigenesis. We discovered that 2 essential endoplasmic reticulum (ER) chaperones, 78-kilodalton glucose-regulated protein (GRP78) and 94-kilodalton glucose-regulated protein (GRP94) have a role in metaplasia. Grp78 haploinsufficiency in the mouse pancreas impairs acinar-to-ductal metaplasia, whereas in the uterus, Grp94 loss induces squamous cell metaplasia; both resulting in tumor suppression.
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Shen et al. (2017) studied this question.
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