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Elevated Sad1 and UNC84 Domain Containing 2 (SUN2) Level Inhibits Cell Growth and Aerobic Glycolysis in Oral Cancer Through Reducing the Expressions of Glucose Transporter 1 (GLUT1) and Lactate Dehydrogenase A (LDHA)

Overview
Journal J Dent Sci
Specialty Dentistry
Date 2021 Jan 1
PMID 33384835
Citations 2
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Abstract

Background/purpose: Oral cancer is a malignant tumor accompanied by high morbidity, mortality, and poor prognosis. Therefore, it is urgent to explore the percise regulation mechanisms underlying oral cancer. Sad1 and UNC84 Domain Containing 2 (SUN2) was considered as a tumor suppressor in some cancers. The purpose of the study was to define the role of SUN2 in oral cancer progression.

Materials And Methods: Tumor tissues and paired paracancerous healthy tissues from 56 oral cancer patients were collected. Cell viability was measured using MTT assay. The colony formation assay was applied to determine cell proliferation ability. The mRNA and protein levels were assessed by qRT-PCR and Western blot, respectively.

Results: SUN2 expression was decreased in oral cancer tissues and cell models. SUN2 overexpression suppressed the growth of oral cancer cells, while the down-regulation of SUN2 promoted cell growth. SUN2 overexpression restrained the glucose uptake, lactate production, and ATP level of oral cancer cells, whereas down-regulation of SUN2 promoted glycolysis. Besides, elevated SUN2 inhibited the glucose transporter 1 (GLUT1) and lactate dehydrogenase A (LDHA) levels. However, SUN2 knockdown increased the levels of GLUT1 and LDHA.

Conclusion: SUN2 was decreased in oral cancer and . SUN2 overexpression suppressed cell growth and glycolysis via reducing the levels of GLUT1 and LDHA in oral cancer.

Citing Articles

Molecular interplay between the upregulated levels of Sad1 and UNC84 Domain Containing 2 (SUN2) and gene expression in medulloblastoma cells.

Tecalco-Cruz A, Macias-Silva M, Sosa-Garrocho M, Poot-Hernandez A, Peralta-Alvarez C, Ramirez-Jarquin J Mol Biol Rep. 2024; 51(1):1164.

PMID: 39560853 DOI: 10.1007/s11033-024-10078-7.


Life outside the LINC complex - Do SUN proteins have LINC-independent functions?.

Belaadi N, Guilluy C Bioessays. 2024; 46(8):e2400034.

PMID: 38798157 PMC: 11262984. DOI: 10.1002/bies.202400034.

References
1.
Chen L, Zhang S, Wu J, Cui J, Zhong L, Zeng L . circRNA_100290 plays a role in oral cancer by functioning as a sponge of the miR-29 family. Oncogene. 2017; 36(32):4551-4561. PMC: 5558096. DOI: 10.1038/onc.2017.89. View

2.
Gatenby R, Gillies R . Why do cancers have high aerobic glycolysis?. Nat Rev Cancer. 2004; 4(11):891-9. DOI: 10.1038/nrc1478. View

3.
Matsumoto A, Hieda M, Yokoyama Y, Nishioka Y, Yoshidome K, Tsujimoto M . Global loss of a nuclear lamina component, lamin A/C, and LINC complex components SUN1, SUN2, and nesprin-2 in breast cancer. Cancer Med. 2015; 4(10):1547-57. PMC: 4618625. DOI: 10.1002/cam4.495. View

4.
Xu Q, Zhang Q, Ishida Y, Hajjar S, Tang X, Shi H . EGF induces epithelial-mesenchymal transition and cancer stem-like cell properties in human oral cancer cells via promoting Warburg effect. Oncotarget. 2016; 8(6):9557-9571. PMC: 5354753. DOI: 10.18632/oncotarget.13771. View

5.
Tamura T, Ichikawa T, Nakahata S, Kondo Y, Tagawa Y, Yamamoto K . Loss of NDRG2 Expression Confers Oral Squamous Cell Carcinoma with Enhanced Metastatic Potential. Cancer Res. 2017; 77(9):2363-2374. DOI: 10.1158/0008-5472.CAN-16-2114. View