Tripartite motif‑containing 11 regulates the proliferation and apoptosis of breast cancer cells

Abstract

Breast cancer, an increasing health problem worldwide, is the second major cause of cancer-associated mortality in females. Studies have focused on the pathogenesis of breast cancer for decades, but the underlying mechanisms have not been fully elucidated. Tripartite motif-containing 11 (TRIM11), a novel oncogene that was recently identified, was reported to function in various types of cancer, including ovarian and lung cancer. In the present study, high expression levels of TRIM11 were detected in breast cancer tissues by reverse transcription-quantitative polymerase chain reaction and western blot analysis, which suggested that TRIM11 was likely to function in the progression of breast cancer. Downregulation of TRIM11 in MCF-7 and MDA-MB-231 cells inhibited cell proliferation and promoted cell apoptosis, accompanied by increased phosphatase and tensin homolog deleted on chromosome 10 (PTEN), p53 and Bcl-2-associated X protein, and decreased B-cell lymphoma 2, phosphorylated c-Jun N-terminal kinase 1/2 (p-JNK1/2) and phosphorylated extracellular signal-regulated kinases 1/2 (p-ERK1/2), whereas the overexpression of TRIM11 completely reversed these effects. Furthermore, TRIM11 downregulation enhanced the pro-apoptotic effect of chemotherapy drugs on breast cancer cells, and high levels of TRIM11 expression were observed in cisplatin- and paclitaxel-resistant breast cancer tissues. These data indicated that TRIM11 is crucial to the development of breast cancer, and TRIM11 downregulation may benefit the treatment of breast cancer by regulating ERK1/2 and JNK1/2 signaling and the expression of apoptosis-associated genes.