Retracted: TPX2 gene silencing inhibits cell proliferation and promotes apoptosis through negative regulation of AKT signaling pathway in ovarian cancer

Abstract

Ovarian cancer (OC) is the leading cause of death from gynecological malignancy. Accumulated studies have revealed that targeting protein for Xklp2 (TPX2) was tightly associated with the development and progression of OC. The present study further determined a novel mechanism of TPX2 in OC via the AKT signaling pathway. The differentially expressed genes were screened in GEO database for gene expression microarray of OC. Bioinformatics was used to analyze the key differentially expressed genes in OC. We prepared CD133/1+ OC stem cells. Then cells were treated with TPX2-1 siRNA and perifcsine to explore the correlation of TPX2 and the AKT signaling pathway. We determined the expression of TPX2, AKT, Pl3 K, PTEN, caspase-3, Bax and Bcl-2 in OC cells. Cell proliferation, migration, invasion, and apoptosis rate were respectively measured using MTT and EdU assays, Transwell assay, Scratch test, and flow cytometry. Xenograft tumor in nude mice was used to determine the effect of TPX2 in OC cells in vitro. Initially, TPX2 overexpression was observed in OC, and TPX2 mediated the effect of the AKT signaling pathway in OC. TPX2 knockdown decreased expression of AKT, Pl3 K, and Bcl-2, and the extent of AKT phosphorylation, but increased expression of PTEN, Caspase-3, and Bax. Furthermore, TPX2 knockdown suppressed OC cell proliferation, migration and invasion, but promoted OC cell apoptosis. Taken together, TPX2 silencing negatively regulates the AKT signaling pathway by which OC cell proliferation was inhibited yet cell apoptosis was accelerated, suggesting a potential therapeutic approach to OC.

TPX2 silencing exerts anti‑tumor effects on hepatocellular carcinoma by regulating the PI3K/AKT signaling pathway

“…The development and progression of HCC are associated with multiple signaling pathways, such as the PI3K/AKT, MAPK/P38, JAK2/STAT3, TGF-β/Smad and NF-κB signaling pathways (22-26). Previous studies have found that TPX2 can regulate the proliferation and apoptosis of a number of different types of malignant tumors via the PI3K/AKT signaling pathway (13,16). In the present study, the potential effects of TPX2 silencing on the expression levels of PI3K/AKT signaling pathway-associated factors in Huh7 or Hep3B cells were assessed.…”

“…However, upregulation of TPX2 can cause centrosome amplification and lead to DNA polyploidy (9). Previous studies have found that TPX2 is upregulated in a wide range of malignant tumors, including esophageal cancer (10), colon cancer (11,12), breast cancer (13), cervical cancer (14,15), ovarian cancer (16), bladder carcinoma (17) and medullary thyroid carcinoma (18). To the best of our knowledge, there are no studies on the association between TPX2 and the occurrence and development of HCC.…”

RHPN1‑AS1 promotes ovarian carcinogenesis by sponging miR‑485‑5p and releasing TPX2 mRNA

“…1B) was significantly upregulated (Fig. 1C) in OC and was partly responsible for cancerous growth in OC (44,48,49). However, researchers are yet to study its effect on OC cells.…”

“…Therefore, TPX2 may provide insights into tumor cell proliferation. Evidence documented in the literature suggested that TPX2 was upregulated in such tumors as cervical cancer, lung cancer, pancreatic ductal adenocarcinomas, bladder cancer, OC and colon cancer (38)(39)(40)(41)(42)(43)(44). More importantly, a recent study revealed that miR-485-3p could suppress colorectal cancer by targeting TPX2 (45).…”

Integrated genomics and comprehensive validation reveal novel drivers of genomic evolution in esophageal adenocarcinoma

“…Role of TPX2, a microtubule associated protein, was also confirmed in HR in EAC cells. TPX2 has been shown to contribute to survival in ovarian 28 and endometrial 29 cancers. Cancer cells with increased genetic instability also show increased sensitivity to suppression of TPX2 30 .…”