Reduced emerin expression marks gastric cancer progression and invasive nuclear remodeling
Altered nuclear morphology is a defining diagnostic feature of malignancy, and nuclear structure is increasingly recognized as a functional regulator of cancer cell invasion. The inner nuclear membrane protein emerin maintains nuclear architecture and restrains invasive phenotypes in breast cancer models, but whether emerin expression is similarly altered in gastric cancer has not been…
Reduced expression of emerin, a protein crucial for maintaining the structure of the nucleus, marks the progression and invasive characteristics of gastric cancer, according to a recent study. Nuclear morphology, which refers to the shape and organization of the nucleus, is a key diagnostic indicator of malignancy, and the role of nuclear structure in cancer cell invasion is becoming more evident.
Emerin, an inner nuclear membrane protein, is known to preserve nuclear architecture and curb invasive traits in breast cancer models, but its role in gastric cancer remains unclear.
Researchers explored the expression of emerin protein, changes in nuclear shape, and restricted migration in noncancerous and malignant gastric cell lines. They also examined emerin protein levels and nuclear envelope positioning across various gastric cancer types using patient tissue samples. Emerin was present at high levels within the nuclear envelope in both cancer-adjacent and noncancerous gastric epithelium, but its presence was diminished in several gastric cancer types, including adenocarcinoma, signet-ring cell carcinoma, mucinous adenocarcinoma, neuroendocrine carcinoma, squamous cell carcinoma, and metastatic lesions.
The study found that reduced levels of emerin at the nuclear envelope were strongly linked to more aggressive tumors, with grade 2 and grade 3 cancers showing significantly lower scores for nuclear envelope compared to noncancerous tissue and grade 1 tumors. Additionally, gastric cancer cell lines AGS and MKN1 exhibited lower emerin protein levels than noncancerous gastric epithelial control cells (HFE-145).
These findings align with previous studies on breast cancer cells, suggesting that gastric cells with decreased emerin expression also have smaller nuclei and increased difficulty migrating through narrow pores.
The findings collectively support the idea that reduced emerin at the nuclear envelope is a consistent characteristic of invasive epithelial tumor progression and a potential biomarker for gastric cancer nuclear remodeling.
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