Abstract
Oral tongue squamous cell carcinoma (OTSCC) is the most common type of oral carcinomas. However, the molecular mechanism by which OTSCC developed is not fully identified. Stromal interaction molecule 1 (STIM1) is a transmembrane protein, mainly located in the endoplasmic reticulum (ER). STIM1 is involved in several types of cancers. Here, we report that STIM1 contributes to the development of human OTSCC. We knocked down STIM1 in OTSCC cell line Tca-8113 with lentivirus-mediated shRNA and found that STIM1 knockdown repressed the proliferation of Tca-8113 cells. In addition, we also showed that STIM1 deficiency reduced colony number of Tca-8113 cells. Knockdown of STIM1 repressed cells to enter M phase of cell cycle and induced cellular apoptosis. Furthermore, we performed microarray and bioinformatics analysis and found that STIM1 was associated with p53 and MAPK pathways, which may contribute to the effects of STIM1 on cell growth, cell cycle, and apoptosis. Finally, we confirmed that STIM1 controlled the expression of MDM2, cyclin-dependent kinase 4 (CDK4), and growth arrest and DNA damage inducible α (GADD45A) in OTSCC cells. In conclusion, we provide evidence that STIM1 contributes to the development of OTSCC partially through regulating p53 and MAPK pathways to promote cell cycle and survival.
Highlights
Oral tongue squamous cell carcinoma (OTSCC) is one of the most common cancers diagnosed in the oral cavity comprising 25–40% of oral carcinomas worldwide [1]
Our microarray data showed that Stromal interaction molecule 1 (STIM1) controlled the p53 and mitogen-activated protein kinase (MAPK) pathways
Our molecular analysis confirmed that STIM1 regulated the protein level of Transformed mouse 3T3 cell double minute 2 (MDM2), cyclin-dependent kinase 4 (CDK4), and growth arrest and DNA damage inducible α (GADD45A)
Summary
Oral tongue squamous cell carcinoma (OTSCC) is one of the most common cancers diagnosed in the oral cavity comprising 25–40% of oral carcinomas worldwide [1]. This type of cancer is well known for its high rate of lymph nodal metastasis and the number of deaths associated with OTSCC increased during the past 5 years [2]. Mutations on the predicted EF hand on residues that are essential for Ca2+ binding attenuate the affinity for Ca2+ and induce constitutive activation of Ca2+ entry even without Ca2+ store depletion [4,5]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
