Anti-EREG (full length) polyclonal antibody

Background/Aim:A great proportion of patients with rectal cancer initially present with locally advanced disease and can potentially benefit from neoadjuvant concurrent chemoradiotherapy (CCRT) for downstaging before surgery. However, risk and clinical outcome stratification remain a great challenge. We aimed to find the potential biomarker to predict the effect of neoadjuvant CCRT on rectal cancer.Methods:We identified epiregulin (EREG) as the most significant predictive marker for neoadjuvant CCRT response from the published rectal cancer transcriptome data set GSE35452. We collected 172 biopsy specimens from rectal cancer patients who received neoadjuvant CCRT followed by radical proctectomy, performed EREG immunohistochemistry, and analyzed the H-scores. We further examined the correlations between the expression level of EREG and clinicopathological features, tumor regression grade, and survival, including disease-specific survival (DSS), locoregional recurrence-free survival (LRFS), and metastasis-free survival (MeFS).Results:High EREG expression was significantly related to early pretreatment (pre-Tx) and posttreatment (post-Tx) tumor status (T1, T2,p= 0.047 andp< 0.001), pre-Tx and post-Tx negative nodal status (N0,p< 0.001 andp= 0.004), less vascular and perineurial invasion (p= 0.015 andp= 0.023), and higher tumor regression grade (p< 0.001). In the survival analysis, high EREG expression was significantly associated with better DSS (p< 0.0001), LRFS (p= 0.0004), and MeFS (p< 0.0001). In the multivariate analysis, high EREG expression remained prognostically significant for better DSS (p= 0.003; hazard ratio: 5.599).Conclusion:These data suggest that EREG is a potential predictive marker and therapeutic target in rectal cancer patients receiving neoadjuvant CCRT.

To investigate the function of epiregulin (EREG) in the migration and chemotaxis ability of mesenchymal stem cells. Adipose-derived stem cells (ADSCs) were used in this investigation. Lentiviral EREG short hairpin RNA was applied to silence EREG expression in ADSCs. Human recombinant EREG protein (rhEREG) was used to perform a gain-of-function study. Scratch-simulated wound migration and transwell chemotaxis assays were used to examine the migration and chemotaxis capacity of ADSCs in vitro. Using a Western blot assay, the expressions of p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase (JNK), extracellular signal-regulated protein kinases 1 and 2 (Erk1/2), and protein kinase B were detected. Depletion of EREG caused by specific short hairpin RNA restrained the migration and chemotaxis ability of ADSCs and inhibited the expressions of phosphorylated p38 MAPK, JNK, and Erk1/2. rhEREG improved ADSCs migration and chemotaxis capacity, which was repressed by knockdown of EREG and rescued the expressions of phosphorylated p38 MAPK, JNK, and Erk1/2 impaired by silencing EREG. Furthermore, rhEREG-improved migration and chemotaxis ability in EREG-depleted-ADSCs was restricted by a specific inhibitor, SB203580, for blocking p38 MAPK signaling, PD98059 for blocking Erk1/2 signaling, or SP600125 for blocking JNK signaling in ADSCs separately. EREG promotes migration and chemotaxis ability of ADSCs through MAPK signaling pathways.