Ovarian cancer (OC) is one of the most common tumors in the female reproductive system and the main cause of death among gynecological tumors [1]. Because of the lack of typical clinical manifestations of early OC, more than 70% of patients were diagnosed at the advanced stage [2]. At present, the standard treatment of OC is cytoreductive surgery combined with platinum-based chemotherapy. Although the prognosis of patients has been greatly improved with the improvement of surgical methods and the progress of neoadjuvant chemotherapy, almost all patients will experience relapse within 5 years after diagnosis and finally become drug resistant [3,4]. Therefore, our goal was to identify a biomarker that may contribute to the prognosis and treatment of OC.

Nuclear atypia has been the hallmark of cancer cells. The poorer the differentiation of cancer cells, the more obvious the nuclear atypia. Therefore, observing the morphological changes of the nucleus is an important basis for differentiating benign and malignant tumors [5,6]. The lamina, a 10–20 nm thick protein reticular structure below the inner nuclear membrane, can attach the chromatin domain to the perinuclear and assist in the fixation of nuclear membrane proteins. The main component of the lamina is lamins, which is a V-type intermediate filament protein. Together with the nuclear membrane to form a nuclear chamber, lamins are involved in a variety of cellular processes including maintaining nuclear shape and integrity, fixing nuclear membrane-associated protein, binding and stabilizing chromatin architecture, participating in the transduction of mechano-signalling, promoting cell cycle progression, regulating gene expression, mitosis, DNA damage repair and DNA replication [[7], [8], [9]]. In mammals, the family of lamin genes includes three different genes, namely LMNA, LMNB1 and LMNB2. According to their sequence homologies, lamins are clarified to A-type and B-type. Studies have shown the function of B-type lamins and found that they are differentially expressed in various tumors[ [10,11]].

LMNB1 and LMNB2, the members of B-type lamins, are translated into lamin B1 and lamin B2 respectively. In combination with other types of lamins, LMNB1 constitutes the nuclear intermediate filaments and helps maintain the integrity of the nucleus[12]. Mutation and replication abnormalities of LMNB1 are associated with syndromic microcephaly, demyelination of the central nervous system, neurological defects and autosomal dominant leukodystrophy [13,14]. Recently, more and more attention has been paid to the function and pathological mechanism of LMNB1 in tumors. LMNB1 is highly expressed in most cancers, and there is a significant correlation between its expression and the prognosis [15,16]. In addition, silencing LMNB1 can inhibit the proliferation and tumor formation of lung adenocarcinoma, and hepatocellular carcinoma [17,18].

In this study, we reported for the first time that LMNB1 serves as a prognostic biomarker for OC and explained the function and molecular mechanism of LMNB1 in the proliferation and migration. We verified the expression level and clinical significance of LMNB1 in OC through public databases and clinical specimens. Then, the study of LMNB1 knockdown revealed the biological functions of LMNB1 on OC in vitro and in vivo assays. Moreover, we explored LMNB1-related signaling pathways through bioinformatics methods and RNA sequencing (RNA-seq). Therefore, these data showed the potential value of LMNB1 as a prognostic biomarker and therapeutic target for OC.