Correction: SPHK1 promotes bladder cancer metastasis via PD-L2/c-Src/FAK signaling cascade.
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Published Erratum↗
Biomedical subjects
Stella Chin-Shaw Tsai
Publications and source records attributed to Stella Chin-Shaw Tsai.
SPHK1 promotes bladder cancer metastasis via PD-L2/c-Src/FAK signaling cascade.
SPHK1 (sphingosine kinase type 1) is characterized as a rate-limiting enzyme in sphingolipid metabolism to phosphorylate sphingosine into sphingosine-1-phosphate (S1P) that can bind to S1P receptors (S1PRs) to initiate several signal transductions leading to cell proliferation and survival of normal cell. Many studies have indicated that SPHK1 is involved in several types of cancer development, however, a little is known in bladder cancer. The TCGA database analysis was utilized for analyzing the clinical relevance of SPHK1 in bladder cancer. Through CRISPR/Cas9 knockout (KO) and constitutive activation (CA) strategies on SPHK1 in the bladder cancer cells, we demonstrated the potential downstream target could be programmed cell death 1 ligand 2 (PD-L2). On the other hand, we demonstrated that FDA-approved SPHK1 inhibitor Gilenya® (FTY720) can successfully suppress bladder cancer metastasis by in vitro and in vivo approaches. This finding indicated that SPHK1 as a potent therapeutic target for metastatic bladder cancer by dissecting the mechanism of action, SPHK1/S1P-elicited Akt/β-catenin activation promoted the induction of PD-L2 that is a downstream effector in facilitating bladder cancer invasion and migration. Notably, PD-L2 interacted with c-Src that further activates FAK. Here, we unveil the clinical relevance of SPHK1 in bladder cancer progression and the driver role in bladder cancer metastasis. Moreover, we demonstrated the inhibitory effect of FDA-approved SPHK1 inhibitor FTY720 on bladder cancer metastasis from both in vitro and in vivo models.
Urinary Bladder Neoplasms↗
Parotid neoplasms: diagnosis, treatment, and intraparotid facial nerve anatomy.
The demographics of parotid neoplasms in different populations have been reported by various centres. In this investigation, we reviewed retrospectively all the in-patient and out-patient charts and records of 108 patients who were diagnosed with parotid neoplasms and received parotidectomies in our department from 1 January 1993 to 15 April 2000. Patient age, gender, tumour pathology, fine-needle aspiration cytology results, and the intraparotid anatomy of the facial nerve were noted. We showed that despite the difference between our Taiwanese and previously studied patient populations, both populations had a similar distribution, diagnosis and treatment of parotid neoplasms, although the incidence of parotid tuberculosis was higher in our patient group. In addition, the facial nerve anatomy within the parotid gland had three main branching patterns in the upper and lower division.
Adenolymphoma↗