Lmnb1, also known as Lamin B1, is a key component of the nuclear skeleton structure. It is involved in various biological processes and may play roles in multiple signaling pathways, though the specific pathways are still being explored. Genetic models, such as gene knockout (KO) and conditional knockout (CKO) mouse models, can be valuable tools to study its functions.

In cancer research, studies on various cancers have shown significant associations. In hepatocellular carcinoma (HCC), Lmnb1 is overexpressed, correlates with pathological stage and poor prognosis, and promotes HCC proliferation in vitro and in vivo by regulating CDKN1A expression [1]. In prostate cancer, while inconsistent results exist, it may play a role in early progression steps [2]. In ovarian cancer, overexpression indicates OC progression, and knockdown inhibits OC cell proliferation and migration by suppressing the FGF1-mediated PI3K-Akt signaling pathway [3]. In lung adenocarcinoma, it is upregulated, correlated with pathological stage and lymphatic metastasis, and its knockdown inhibits tumor development [4]. In addition, in lung cancer, Lmnb1 can activate GPR84 through the JAK-STAT pathway to mediate M2 macrophage polarization [5].

In conclusion, Lmnb1 is crucial for the nuclear skeleton structure and is involved in cancer-related biological processes. Model-based research, especially KO/CKO mouse models, has revealed its role in promoting the progression of multiple cancers, providing potential therapeutic targets and prognostic biomarkers for these diseases.