Mki67
Mki67
Overview
Mki67 encodes Ki-67, a widely used nuclear protein and canonical marker of cellular proliferation. In pathology and experimental biology, Ki-67 immunostaining is commonly used to estimate the fraction of actively cycling cells, making it an important biomarker in tumor grading, prognosis, and treatment response assessment. Although often treated as a proliferation readout rather than a direct therapeutic target, Ki-67 expression is frequently analyzed alongside cell-cycle regulators such as CDK1, CCNA2, CCNB1, and Cdk4/6-related pathways, as well as signaling networks including MAPK, PI3K/AKT/mTOR, Ras/Raf/MEK/ERK, AMPK, and JAK/STAT.
Recent studies continue to use Mki67 as a marker of tumor growth, tissue regeneration, and drug response across cancer, wound healing, and organ repair models. In this context, reduced Ki-67 staining generally indicates suppressed proliferation or therapeutic efficacy, whereas increased Ki-67 positivity is interpreted as enhanced regenerative or proliferative activity depending on the biological setting.
Focus of Latest Publications
Recent publications have continued to evaluate Mki67/Ki-67 primarily as a proliferation-associated biomarker, with growing interest in whether its expression can be predicted noninvasively and how it relates to tumor aggressiveness and treatment response. In hepatocellular carcinoma, a dual-center study used T2-weighted MRI habitat analysis to link T2WI-derived parameters with Ki-67 status and aggressiveness. A separate computational study of BPA-related hepatocarcinogenesis identified MKI67 among six hub genes upregulated in hepatocellular carcinoma, with high internal diagnostic accuracy reported for the gene set, although the authors noted that external validation is still needed.
Several recent studies focused on imaging- and deep learning-based prediction of Ki-67 expression in solid tumors. In gliomas, a multimodal ConvNeXt-Tiny deep learning model was developed to simultaneously predict IDH mutation status and Ki-67 expression level. In breast cancer, Ki-67 was examined as a predictor of pathological complete response and invasive disease-free survival in HER2-positive disease, while another large prospective observational analysis in hormone receptor-positive/HER2-negative early breast cancer assessed clinical and molecular predictors of endocrine therapy response after short preoperative treatment, noting that low Ki-67 after endocrine therapy indicates a favorable prognosis.
Beyond its use as a biomarker, one study reported a functional role for Ki-67 in metastasis. Using single-cell transcriptomics of circulating tumor cells and in vivo CRISPR screening in breast cancer mouse models, investigators found that Ki-67 was required for circulating tumor cell intravasation and metastatic competence. Ki-67 knockout reduced metastasis without curbing proliferation, and the effect was linked to reduced expression of genes involved in cell-cell adhesion, including CD47 and KLF4, suggesting a role in collective invasion dynamics rather than proliferation alone.
Ki-67 was also incorporated into studies of tumor biology and pathology in other settings. In pancreatic ductal adenocarcinoma, a mouse model of intrapancreatic fat deposition showed increased MKI67 expression alongside FABP5 upregulation and activation of JAK/STAT, PI3K/AKT/mTOR, and Ras/Raf/MEK/ERK signaling pathways, with associated acceleration of tumor growth and metastasis. In diffuse large B-cell lymphoma, a prospective observational study compared dose-adjusted EPOCH-R with R-CHOP in patients with high Ki-67 expression. In hepatic neuroendocrine tumors, Ki-67 was listed among key biomarkers used in diagnosis and treatment planning. In a nail tumor study, normal Ki67 expression helped rule out in situ onycholemmal carcinoma/malignant onychopapilloma, supporting the benign diagnosis.