Apigenin is a natural flavonoid that exhibits anti-proliferative activity and induces apoptosis in various types of cancer, including colon cancer. The aim of the present study was to determine the mechanism underlying the apoptosis-inducing effect of apigenin in colon cancer. Apigenin reduced the proliferation of colon cancer cell lines, stimulated the cleavage of PARP and induced apoptosis in a dose-dependent manner. Apigenin treatment also suppressed the expression of the anti-apoptotic proteins Bcl-xL and Mcl-1. Small interfering RNA was used to knockdown Bcl-xL and Mcl-1 expression alone and in concert, and the proliferation and apoptosis of cancer cells were subsequently measured. The knockdown of Bcl-xL and Mcl-1 expression together markedly suppressed cell proliferation and induced apoptosis. Apigenin treatment also inhibited the phosphorylation of signal transducer and activator of transcription 3 (STAT3), which targets Bcl-xL and Mcl-1. The results of the current study therefore determined that apigenin induces the apoptosis of colon cancer cells by inhibiting the phosphorylation of STAT3 and consequently downregulates the anti-apoptotic proteins Bcl-xL and Mcl-1.

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Abstract. Girdin, an actin-binding Akt substrate, regulates actin reconstruction and Akt-dependent cell motility in fibroblasts and in a human breast cancer cell line. We examined whether Girdin is also involved in the motility of esophageal squamous cell carcinoma (ESCC) cells. Immunofluorescent staining and migration assays were performed, using KYSE cell lines, to examine whether Girdin is involved in the motility of ESCC cells. Upon EGF stimulation, Girdin colocalized with filamentous actin (F-actin) in the lamellipodia as determined by immunofluorescent staining. In migration assays, cell motility was significantly reduced in KYSE cell lines transfected with Girdin siRNA compared with the negative control. In addition, we examined the relationship between Girdin expression and clinical data, using specimens resected from ESCC patients. In immunohistochemical (IHC) analyses using specimens resected from ESCC patients, overall survival was significantly longer in cases showing lower Girdin expression compared to cases with higher Girdin expression. Collectively, Girdin appears to be involved in the motility of ESCC cells. The levels of Girdin expression correlated inversely with the survival of ESCC patients. Therefore, in ESCC, Girdin may be a prognostic marker and may serve as a therapeutic target as well.

An aneurysm of the middle-colic artery, associated with segmental arterial mediolysis (SAM), is a rare condition. This report describes a case of a middle-colic artery aneurysm that was associated with SAM. A 57-year-old man was admitted to our hospital because of severe abdominal pain. A rupture of a middle-colic artery aneurysm was diagnosed by computed tomography, and angiography showed that it may have been associated with SAM. The ruptured aneurysm was successfully treated with transcatheter arterial embolization. Transcatheter arterial embolization might be one of the best treatments for such a complicated aneurysm occurring in a visceral artery.