The B-cell translocation gene 3 (BTG3) is a member of the antiproliferative BTG gene family and a downstream target of p53. BTG3 also binds and inhibits E2F1. Although it connects functionally two major growth-regulatory pathways, the physiological role of BTG3 remains largely uncharacterized. Here, we present evidence that loss of BTG3 in normal cells induced cellular senescence, which was correlated with enhanced ERK-AP1 signaling and elevated expression of the histone H3K27me3 demethylase JMJD3/KDM6B, leading to acute induction of p16(INK4a). Importantly, we also found that BTG3 expression is specifically downregulated in prostate cancer, thus providing a physiological link with human cancers. Our data suggest that BTG3 may have a fail-safe role against tumorigenic progression.

BTG3 (B-cell translocation gene 3) is a p53 target that also binds and inhibits E2F1. Although it connects two major growth-regulatory pathways functionally and is downregulated in human cancers, whether and how BTG3 acts as a tumor suppressor remain largely uncharacterized. Here we present evidence that BTG3 binds and suppresses AKT, a kinase frequently deregulated in cancers. BTG3 ablation results in increased AKT activity that phosphorylates and inhibits glycogen synthase kinase 3β. Consequently, we also observed elevated β-catenin/T-cell factor activity, upregulation of mesenchymal markers, and enhanced cell migration. Consistent with these findings, BTG3 overexpression suppressed tumor growth in mouse xenografts, and was associated with diminished AKT phosphorylation and reduced β-catenin in tissue specimens. Significantly, a short BTG3-derived peptide was identified, which recapitulates these effects in vitro and in cells. Thus, our study provides mechanistic insights into a previously unreported AKT inhibitory pathway downstream of p53. The identification of an AKT inhibitory peptide also unveils a new avenue for cancer therapeutics development.

Carcinoembryonic antigen (CEA) titre elevation is sometimes found in benign diseases, such as gastro-intestinal tract inflammatory disease and chronic obstructive pulmonary disease; however, very high CEA titre is rarely encountered in benign pulmonary disease.A 36-yr-old female, who had suffered from body weight loss, was found to have high serum CEA titre (60.8 ng?mL -1). Image studies revealed one pulmonary tumour at the left lower lobe, satellite nodules and mediastinal lymphadenopathy.Left lower lobectomy and lymph node dissection were performed for suspicious pulmonary malignancy. The pathological examination revealed that the tumourous lesion was composed of small and fragmented foreign bodies, fibrinopurulent exudate and heavy eosinophils. The bronchial epithelium was characterised by goblet cell hyperplasia and CEA overexpression. The remaining lung parenchyma possessed similar foreign body reaction. The patient's medical history was reviewed and it was found that she had spread propolis topically on nasal mucosa as an adjuvant therapy to asthma for 6 months prior to this medical event. The CEA titre decreased after the operation to 14.2 and 7.88 ng?mL -1 after 2 weeks and 6 months, respectively.Propolis is used widely in folk medicine but it also has strong sensitising potential. One rare case of propolis aspiration is reported with presentation mimicking lung cancer.

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