An Unusual Complication of Self-Expandable Metal Stent Placement in Malignant Sigmoid Obstruction.

Self-expandable metal stent (SEMS) for malignant colorectal obstruction is widely used as a bridge to elective surgery or palliative treatment. However, with the increasing use of SEMS for treatment, complication rates associated with stents have been raised as a concern. We experienced a rare migration-related complication that a stent partially migrated out of the anus with an incarceration. A 62-year-old man was admitted with sigmoid malignant obstruction. Due to multiple metastases, he refused to undergo colostomy, and an uncovered SEMS was placed. Subsequently, he started chemotherapy. Seven months after placement, the stent migrated into the rectum. After unsuccessful attempts to extract the stent, he sought our assistance. We observed that half of the stent was outside the anus, and a 15 mm lump of mucosa was embedded in the proximal end of the stent. After several attempts, we successfully removed the SEMS. Stent incarceration following migration is not a common occurrence, but it serves as a reminder that clinicians need to be more vigilant about complications that may arise after stent implantation. We describe this unusual complication and share our experience about the removal of the stent.

Endoscopic incision of rectal diverticulum: A case report.

A 70-year-old woman with a rectal diverticulum presented with anal pendant expansion and difficulty in defecation for more than 1 year. The patient was diagnosed with a rectal diverticulum by pelvic enhanced magnetic resonance imaging (MRI), computerized tomography (CT), rectal angiography, and colonoscopy. The endoscopic diverticulum incision procedure (EDIP) was implemented with this patient. At the 4-month follow-up, anal pendant expansion and difficulty in defecation were significantly relieved. Furthermore, colonoscopy proved that there were no vestigial feces in the diverticulum.

Calcium Channel Protein ORAI1 Mediates TGF-ß Induced Epithelial-to-Mesenchymal Transition in Colorectal Cancer Cells.

Accumulating evidence suggested that calcium release-activated calcium modulator 1(ORAI1), a key calcium channel pore-forming protein-mediated store-operated Ca2+ entry (SOCE), is associated with human cancer. However, its role in colorectal cancer (CRC) progression has not been well studied. Epithelial-mesenchymal transition (EMT) is a multistep process that occurs during the progression of cancers and is necessary for metastasis of epithelial cancer. Transforming growth factor-ß (TGF-ß) is a pleiotropic cytokine that has been shown to induce EMT. In this study, we are aimed at exploring the effects of ORAI1 on TGF-ß1-induced EMT process in CRC cells. Herein, we confirmed ORAI1 expression was higher in CRC tissues than in adjacent non-cancerous tissues by using immunohistochemical staining and Western blot analysis. Higher ORAI1 expression was associated with more advanced clinical stage, higher incidence of metastasis and shorter overall survival. We compared ORAI1 expression in SW480 and SW620 cells, two CRC cell lines with the same genetic background, but different metastatic potential. We found ORAI1 expression was significantly higher in SW620 cells which exhibited higher EMT characteristics. Furthermore, knockdown of ORAI1 suppressed the EMT of SW620 Cells. After induced the EMT process in SW480 cells with TGF-ß1, we found treatment of TGF-ß1 showed a significant increase in cell migration along with the loss of E-cadherin and an increase in N-cadherin and Vimentin protein levels. Also, TGF-ß1 treatment increased ORAI1 expression and was closely associated with the increase of SOCE. Silencing ORAI1 significantly suppressed Ca2+ entry, reversed the changes of EMT-relevant marks expression induced by TGF-ß1, and inhibited TGF-ß1-mediated calpain activation and cell migration. Finally, we blocked SOCE with 2-APB (2-Aminoethyl diphenylborinate), a pharmacological inhibitor. Interestingly, 2-APB and sh-ORAI1 both exhibited similar inhibition effects to the SW480 cells. In conclusion, our results demonstrated that ORAI1 could mediate TGF-ß-Induced EMT by promoting Ca2+ entry and calpain activity in Colorectal Cancer Cells.