The poor prognosis of patients with pancreatic ductal adenocarcinoma (PDAC) is partially attributed to the invasive and metastatic behavior of this disease. Laminin subunit beta-3 (LAMB3) encodes one of the three subunits of LM-332, an extracellular matrix protein secreted by cultured human keratinocytes. In addition, LAMB3 is involved in the invasive and metastatic abilities of some types of cancer, including colon, pancreas, lung, cervix, stomach, and prostate cancer, but the role and mechanism of LAMB3 in PDAC have not been previously determined. Herein, we tentatively investigated the role of LAMB3 in the malignant biological behavior of PDAC. In this study, we demonstrated that LAMB3 is upregulated in PDAC. Inhibition of LAMB3 abrogated the tumorigenic outcomes of PI3K/Akt signaling pathway activation, including those involving cell cycle arrest, cell apoptosis, proliferation, invasion and migration in vitro, and tumor growth and liver metastasis in vivo. Our results showed that LAMB3 could mediate cell cycle arrest and apoptosis in PDAC cells and alter the proliferative, invasive, and metastatic behaviors of PDAC by regulating the PI3K/Akt signaling pathway. LAMB3 may be a novel therapeutic target for the treatment of PDAC in the future.

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Long non-coding RNAs (lncRNAs) refer to functional cellular RNAs molecules longer than 200 nucleotides in length. Unlike microRNAs, which have been widely studied, little is known about the enigmatic role of lncRNAs. However, lncRNAs have motivated extensively attention in the past few years and are emerging as potentially important regulators in pathological processes, including in cancer. We now understand that lncRNAs play role in cancer through their interactions with DNA, protein, and RNA in many instances. Moreover, accumulating evidence has recognized that large classes of lncRNAs are functional for ovarian cancer. Nevertheless, the biological phenomena and molecular mechanisms of lncRNAs in ovarian cancer remain to be better identified. In this review, we outline the dysregulated expression of lncRNAs and their potential clinical implications in ovarian cancer, with a particular emphasis on discussing the well characterized mechanisms underlying lncRNAs in ovarian cancer.

Thalidomide and lenalidomide improve mural cell coverage of bAVM vessels and reduce bAVM hemorrhage, which is likely through upregulation of Pdgfb expression.