Abstract

 
 
 
 Purpose: To investigate the effect of cell division cycle associated 8 (CDCA8) on malignant progression of gastric cancer (GC) cells.
 Methods: Short hairpin RNAs (shRNA) were transfected into two gastric cell lines to knock down expression of CDCA8. Transfection efficiency was analyzed using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Then, Cell Counting Kit 8 and colony formation and Transwell assays were utilized to explore the effect of CDCA8 knockdown on the proliferation, invasion, and migration of GC cells. Flow cytometry was conducted to analyze the effect of CDCA8 knockdown on cell cycle progression and apoptosis. The relationship between CDCA8, epithelial-mesenchymal transition (EMT), and Akt pathway activity was determined by western blot analysis.
 Results: Proliferation, invasion, and migration of GC cells were significantly inhibited by CDCA8 knockdown. Knockdown of CDCA8 induced cell cycle arrest in G1 phase and apoptosis, and inhibited EMT and Akt pathway activity.
 Conclusion: Knockdown of CDCA8 inhibits GC growth and metastasis in vitro by reducing Akt pathway activity. Thus, this molecule presents a potential strategy for the management of GC.
 
 
 
Highlights
Gastric cancer (GC) is one of the most aggressive common malignancies, with approximately 1,000,000 new cases and 781,000 deaths according to global cancer statistics in 2018 [1]
cell division cycle associated 8 (CDCA8) is often reported as an oncogene, which suggests that CDCA8 may promote the malignant growth of GC
Knockdown of CDCA8 may induce cell cycle arrest. This speculation was tested using flow cytometry, which showed that CDCA8 knockdown induced cell cycle arrest in G1 phase (Figure 2 A)
Summary
Gastric cancer (GC) is one of the most aggressive common malignancies, with approximately 1,000,000 new cases and 781,000 deaths according to global cancer statistics in 2018 [1]. GC progresses rapidly to advanced stages, and the high recurrence rate and high invasiveness of advanced GC are the main causative factors of patient deaths. The mechanisms that drive cancer occurrence and metastasis include those that promote proliferation, migration, invasion, and angiogenesis, and lead cells to evade aging and CDCA8 targets CPC components to the centrosome, corrects kinetochore attachment errors, and stabilizes the bipolar axis of human cells, and has important regulatory functions during mitosis [6,9,10]. Overexpression of CDCA8 is associated with malignant progression of cancer and poor patient prognosis in a variety of human cancers, including pancreatic ductal adenocarcinoma [11] and lung cancer [12]. CDCA8 is considered a potential new therapeutic target and prognostic marker for cancer
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