Ubiquitin-specific protease 21 (USP21) has been implicated in several types of cancer.It promotes or suppresses tumor growth in a cell-context dependent manner. Cholangiocarcinoma is a malignant tumor with a high mortality rate. However, the role of USP21 in cholangiocarcinoma remains unknown. Here, we identify that the level of USP21 is upregulated in cholangiocarcinoma using bioinformatics analysis and confirm this elevation in RBE cell lines. Cell counting and 5-ethynyl-2′-deoxyuridine incorporation assays reveal that USP21 promotes the proliferation of cholangiocarcinoma.Wound healing and transwell assays demonstrate that USP21 accelerates RBE cell migration. In addition, rescue assays reveal that reintroduction of USP21 wildtype other than the deubiquitinase-deficient C221A mutant restores USP21 depletioninduced attenuation in cell proliferation and migration, indicative of the requirement of the deubiquitinase activity. Collectively, these data indicate that USP21 is critically involved in cholangiocarcinoma tumorigenesis and may be an effective target for the treatment of cholangiocarcinoma.

Non-small cell lung cancer (NSCLC) is the most common cause of cancer mortality worldwide. NSCLC has an aggressive phenotype and poor prognosis, and is quite heterogeneous without effective and specific targeted therapies. Therefore, exploring new tumor markers and drug targets for NSCLC is crucial towards individualized treatment. Here, we demonstrate that enkurin domain containing 1 (ENKD1), a protein with unknown structure and function, is significantly downregulated in NSCLC tumor tissues compared with their non-tumor counterparts. We also show that ENKD1 expression is decreased in NSCLC cells compared to normal human lung epithelial cells. EdU incorporation, wound healing, and transwell invasion assays reveal that ENKD1 regulates the proliferation, migration, and invasion of NSCLC cells. Collectively, these results suggest that ENKD1 plays an important role in NSCLC progression and that ENKD1 is a tumor marker and a potential molecular drug target for the treatment of NSCLC patients.

Retinal pigment epithelium (RPE) is a highly polarized epithelial monolayer lying between the photoreceptor layer and the Bruch membrane. It is essential for vision through participating in many critical activities, including phagocytosis of photoreceptor outer segments, recycling the visual cycle‐related compounds, forming a barrier to control the transport of nutrients, ions, and water, and the removal of waste. Primary cilia are conservatively present in almost all the vertebrate cells and acts as a sensory organelle to control tissue development and homeostasis maintenance. Numerous studies reveal that abnormalities in RPE lead to various retinal diseases, such as age‐related macular degeneration and diabetic macular oedema, but the mechanism of primary cilia in these physiological and pathological activities remains to be elucidated. Herein, we summarize the functions of primary cilia in the RPE development and the mutations of ciliary genes identified in RPE‐related diseases. By highlighting the significance of primary cilia in regulating the physiological and pathological processes of RPE, we aim to provide novel insights for the treatment of RPE‐related retinal diseases.