Aberrant Expression of BUB1B Contributes to the Progression of Thyroid Carcinoma and Predicts Poor Outcomes for Patients

Abstract

Objective: This study aimed to clarify the function and potential mechanism of BUB1B in THCA. Methods: Expression of BUB1B in THCA was firstly determined, and its important prognostic value was then demonstrated. The potential mechanism was initially predicted by KEGG analysis. To explore the specific function of BUB1B in THCA, we used lentivirus infection to knock down the BUB1B, and then performed flow cytometry, colony formation, transwell, and wound-healing assays. Related protein expression was detected through western blotting. Additionally, we predicted the BUB1B-regulated pathways involved in THCA by GSEA analysis. Results: BUB1B expression was highly increased in THCA tissues relative to normal controls. We further found that BUB1B was essential for tumor cell proliferation, and BUB1B high expression predicted a shorter PFS time of THCA patients. More importantly, Cox regression determined the BUB1B as an independent prognostic factor for PFS in THCA. BUB1B was initially found to participate in the cell cycle pathway from KEGG analysis. Unexpectedly, we did not detect the disturbing effect on the cell cycle distribution of THCA cells with BUB1B knockdown. But, BUB1B knockdown inhibited the proliferation, invasion, and migration of THCA cells, as well as increased apoptotic cells, and the results were further confirmed by western blotting. Through GSEA analysis, we predicted a positive correlation between BUB1B and metastasis-related pathways such as mTOR and NF-kappa B signaling pathways. Conclusions: Present study identified BUB1B as a promising clinical prognostic factor in THCA, as well as a potential novel therapeutic target for cancer treatment.

A whole-genome CRISPR screen identifies the spindle accessory checkpoint as a locus of nab-paclitaxel resistance in pancreatic cancer cells

“…Taken together, these results suggest that the TTK inhibitor may rescue the cells from the apoptotic effects of paclitaxel. BUB1B, BUB3, or TTK overexpression has no effect on the sensitivity of PANC-1 cells to nabpaclitaxel treatment Overexpression of the SAC gene has been observed in various cancers, including pancreatic, thyroid, prostate, and liver cancers [38][39][40][41] . Our study found that overexpression of the three SAC genes (BUB1B, TTK, and BUB3) does not significantly affect sensitivity to nab-abraxane.…”

“…Overexpression of the SAC gene has been observed in various cancers, including pancreatic, thyroid, prostate, and liver cancers [38][39][40][41] . Our study found that overexpression of the three SAC genes (BUB1B, TTK, and BUB3) does not significantly affect sensitivity to nab-abraxane.…”

Identification of molecular subtypes, risk signature, and immune landscape mediated by necroptosis-related genes in non-small cell lung cancer

“…In this research, we used the previous cDNA to conduct a qRT-PCR assay in Light Cycler 480II (Roche, Basel, Switzerland) using SYBR Green technology (Takara), and primer sequences were obtained from a primer bank. Primer sequences were from previous references (28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39) and primer bank (https://pga.mgh.harvard.edu/primerbank/). In addition, 2 −Dct was used to normalize and simplify to generate a riskscore.…”