CacyBP/SIP protein is important for the proliferation of human glioma cells

Abstract

Recently, calcyclin-binding protein or Siah-1-interacting protein (CacyBP/SIP), a component of a novel ubiquitinylation pathway, could regulate the b-catenin degradation (Fukushima et al., Immunity 2006, 24, 29 -39). However, the potential role of CacyBP/SIP itself in human glioma cells has not been clarified. Here, we found that CacyBP/SIP was expressed highly in human glioma tissues. Silencing of CacyBP/SIP by short-hairpin RNA severely suppressed the proliferation of human glioma cell U251, which was at least partly mediated by downregulation of phospho-Akt (p-Akt) and phospho-b-catenin (p-b-catenin) as well as upregulation of p53 and p21. Furthermore, overexpression of CacyBP/SIP obviously promoted the proliferation of human glioma U251, which exhibited the exactly contrary trend in the expression of p-Akt, p-b-catenin, p53, and p21. Taken together, these findings suggest that CacyBP/SIP plays important roles in the proliferation of human glioma cell which might be involved in the development of human glioma. V C 2014 IUBMB Life, 66(4): [286][287][288][289][290][291] 2014

CacyBP/SIP inhibits the migration and invasion behaviors of glioblastoma cells through activating Siah1 mediated ubiquitination and degradation of cytoplasmic p27

“…Shi et al (2014) have showed that CacyBP/SIP is increasingly expressed in human glioma tissues and functions as a promoting factor in glioma cell proliferation; however, the effects of CacyBP/SIP on human glioma cell migration and invasion have not been elaborated. The quantitative data were displayed by means AE S.E.M.…”

“…The construction of stable cell lines was carried out as Shi et al previously described (Shi et al, 2014;Zou et al, 2016). For stably knocking down or overexpressing of CacyBP/SIP, the U251 and U87 cells were infected by Control, shCacyBP/ SIP, GFP, GFP-CacyBP/SIP lentiviruses, respectively.…”

“…Then, we explored whether the behaviors of migration and invasion will be inhibited by overexpressing of CacyBP/SIP. These CacyBP/SIP promotes the ubiquitination and degradation of cytoplasmic p27 Shi et al (2014) reported that CacyBP/SIP is increasingly expressed in glioma patients and plays a role in promoting the glioma cell proliferation. The transwell invasion assay indicated that the number of invasive cells was approximately reduced by 75 AE 6 and 78 AE 8% in U251 and U87 cells, respectively ( Figures 4D-4F).…”

Overexpression of RASD1 inhibits glioma cell migration/invasion and inactivates the AKT/mTOR signaling pathway

“…The RASD1 lentivirus plasmid was constructed, produced and used to infect the glioma cells as described in our previous publication 28, 29 . Forty-eight hours after infection, the virus-infected cells were cultured in the medium containing 2.5 μg/mL puromycin (Sigma, St. Louis, MO) for selection.…”

Nrdp1S, short variant of Nrdp1, inhibits human glioma progression by increasing Nrdp1‐mediated ErbB3 ubiquitination and degradation

“…Nrdp1 has potent auto‐ubiquitination activity, which leads to its constitutive degradation and short half‐life in transformed cells 11, 17. Nrdp1 auto‐ubiquitination was also shown to be dependent on the formation of Nrdp1–Nrdp1 homodimers involving the coiled‐coil domains of the proteins 19.…”