[Expression and significance of pepsin in lingual tonsil hypertrophy].

Objective: To discuss the relationship between lingual tonsil hypertrophy and laryngopharyngeal reflux. Methods: Ninety-two patients who received throat surgery in Nanfang Hospital between October 2015 and October 2016 were enrolled. Twenty-six healthy volunteers were recruited as normal controls. All participants were assessed with the reflux finding score(RFS) and the size of lingual tonsils were evaluated using a clinical grading system proposed by Friedman under electronic laryngoscope. The score of reflux symptom index(RSI), personal history and medical history were gathered. Biopsy specimens of lingual tonsils were taken from all participants for the immunohistochemical stain of pepsin.SPSS 19.0 software was used for statistical analysis. Results: There were 46.2% (12/26) pepsin-positive and 53.8% (14/26) pepsin-negative volunteers in normal controls. There were 87.0% (80/92) pepsin-positive and 13.0% (12/92) pepsin-negative patients in study group. The severity of lingual tonsil hypertrophy and expression intensity of pepsin in patients were significantly higher in volunteers (Z=-3.636, Z=-5.273, P<0.01). The severity of lingual tonsil hypertrophy was positively associated with the pepsin level in patients (r=0.556, P<0.01). The patients with pepsin-positive expression showed significant correlation between lingual tonsil hypertrophy and the positive rate of RSI and RFS (r=0.258, r=0.225, P<0.05). Analysis of correlated factors indicated that lingual tonsil hypertrophy was associated with smoking (χ(2)=8.502, P<0.05). Conclusions: The expression of pepsin can be detected in lingual tonsil tissues. The lingual tonsil hypertrophy is closely related to laryngopharyngeal reflux.

Cross-talk between endothelial cells and tumor via delta-like ligand 4/Notch/PTEN signaling inhibits lung cancer growth.

Lung cancer is a leading cause of cancer death in many countries. Notch signaling has been demonstrated to frequently participate in the process of lung carcinogenesis. Delta-like ligand 4 (Dll4) is a vascular-specific ligand of Notch, and has a critical role in the angiogenesis of numerous cancers. However, the role of Dll4 in the cross-talk between endothelial cells (ECs) and tumor cells remains obscure. Herein, our study revealed that Dll4-expressing ECs (EC-Dll4) significantly suppressed the proliferation of neighboring non-small cell lung cancer (NSCLC) cells and attenuated the growth of NSCLC xenograft in nude mice. On the contrary, silencing endothelial Dll4 by its specific interference RNA reversed these effects of Dll4 on NSCLC cell proliferation and tumor formation. Furthermore, activation of Notch1, but not Notch2 or Notch3, was enhanced in NSCLC cells cultured with EC-Dll4, as well as in xenografts induced by a mixture of NSCLC cells and EC-Dll4. Interference of Notch1 significantly attenuated Dll4-mediated suppression of NSCLC cell proliferations, indicating that Dll4/Notch1 signaling negatively modulates the NSCLC growth. Moreover, PTEN expression in NSCLC cells was increased by EC-Dll4 or rhDll4 (recombinant human-Dll4 protein), and the induction was impaired by Notch1 interference suggesting that Dll4 could upregulate PTEN expression by Notch1. Taken together, we conclude that the cross-talk between ECs and NSCLC cells by Dll4/Notch1/PTEN signaling pathway inhibits the growth of NSCLC.