BACKGROUND Monopolar spindle-binding protein 3B(MOB3B)functions as a signal transducer and altered MOB3B expression is associated with the development of human cancers.AIM To investigate the role of MOB3B in colorecta...BACKGROUND Monopolar spindle-binding protein 3B(MOB3B)functions as a signal transducer and altered MOB3B expression is associated with the development of human cancers.AIM To investigate the role of MOB3B in colorectal cancer(CRC).METHODS This study collected 102 CRC tissue samples for immunohistochemical detection of MOB3B expression for association with CRC prognosis.After overexpression and knockdown of MOB3B expression were induced in CRC cell lines,changes in cell viability,migration,invasion,and gene expression were assayed.Tumor cell autophagy was detected using transmission electron microscopy,while nude mouse xenograft experiments were performed to confirm the in-vitro results.RESULTS MOB3B expression was reduced in CRC vs normal tissues and loss of MOB3B expression was associated with poor CRC prognosis.Overexpression of MOB3B protein in vitro attenuated the cell viability as well as the migration and invasion capacities of CRC cells,whereas knockdown of MOB3B expression had the opposite effects in CRC cells.At the molecular level,microtubule-associated protein light chain 3 II/I expression was elevated,whereas the expression of matrix metalloproteinase(MMP)2,MMP9,sequestosome 1,and phosphorylated mechanistic target of rapamycin kinase(mTOR)was downregulated in MOB3B-overexpressing RKO cells.In contrast,the opposite results were observed in tumor cells with MOB3B knockdown.The nude mouse data confirmed these in-vitro findings,i.e.,MOB3B expression suppressed CRC cell xenograft growth,whereas knockdown of MOB3B expression promoted the growth of CRC cell xenografts.CONCLUSION Loss of MOB3B expression promotes CRC development and malignant behaviors,suggesting a potential tumor suppressive role of MOB3B in CRC by inhibition of mTOR/autophagy signaling.展开更多
Colorectal cancer(CRC)is a common malignancy that has the second highest incidence and mortality rate.Although there are many personalized treatment options for CRC,the therapeutic effects are ultimately limited by dr...Colorectal cancer(CRC)is a common malignancy that has the second highest incidence and mortality rate.Although there are many personalized treatment options for CRC,the therapeutic effects are ultimately limited by drug resistance.Studies have aimed to block the initiation and progression of CRC by inducing cell death to overcome this obstacle.Substantial evidence has indicated that both autophagy and ferroptosis play important regulatory roles in CRC.Autophagy,a lysosome-dependent process by which cellular proteins and organelles are degraded,is the basic mechanism for maintaining cell homeostasis.The duality and complexity of autophagy in cancer therapy is a hot topic of discussion.Ferroptosis,a regulated cell death pathway,is associated with iron accumulationinduced lipid peroxidation.The activation of ferroptosis can suppress CRC proliferation,invasion and drug resistance.Furthermore,recent studies have suggested an interaction between autophagy and ferroptosis.Autophagy can selectively degrade certain cellular contents to provide raw materials for ferroptosis,ultimately achieving antitumor and anti-drug resistance.Therefore,exploring the interaction between autophagy and ferroptosis could reveal novel ideas for the treatment of CRC.In this review,we describe the mechanisms of autophagy and ferroptosis,focusing on their roles in CRC and the crosstalk between them.展开更多
BACKGROUND Small intestinal cavernous hemangioma is a rare disease,especially in the ileum.It is difficult to accurately diagnose due to its hidden location and nonspecific clinical symptoms.Here,we reported a case of...BACKGROUND Small intestinal cavernous hemangioma is a rare disease,especially in the ileum.It is difficult to accurately diagnose due to its hidden location and nonspecific clinical symptoms.Here,we reported a case of ileal cavernous hemangioma with chronic hemorrhage in a 20-year-old man and review the literature to gain a better understanding of this disease.CASE SUMMARY The patient complained of intermittent melena and hematochezia for > 3 mo.The lowest hemoglobin level revealed by laboratory testing was 3.4 g/d L(normal range:12-16 g/dL).However,the gastroscopy,colonoscopy and peroral doubleballoon enteroscopy(DBE) showed no signs of bleeding.The transanal DBE detected a lesion at about 340 cm proximal to the ileocecal valve.Thus,we performed an exploratory laparoscopy and the lesion was resected.After the operation,the patient had no melena.Finally,the pathological examination identified the neoplasm as an ileal cavernous hemangioma,thereby resulting in gastrointestinal hemorrhage.CONCLUSION This report might improve the diagnosis and treatment of ileal cavernous hemangioma.展开更多
基金Supported by National Natural Science Foundation of China,No.81760516Natural Science Foundation of Guangxi,China,No.2019GXNSFAA185030+1 种基金Self-Financed Scientific Research Projects of Guangxi Zhuang Autonomous Region Health and Family Planning Commission,China,No.Z20181003Guangxi Medical University Youth Science Fund Project,China,No.GXMUYSF202221.
文摘BACKGROUND Monopolar spindle-binding protein 3B(MOB3B)functions as a signal transducer and altered MOB3B expression is associated with the development of human cancers.AIM To investigate the role of MOB3B in colorectal cancer(CRC).METHODS This study collected 102 CRC tissue samples for immunohistochemical detection of MOB3B expression for association with CRC prognosis.After overexpression and knockdown of MOB3B expression were induced in CRC cell lines,changes in cell viability,migration,invasion,and gene expression were assayed.Tumor cell autophagy was detected using transmission electron microscopy,while nude mouse xenograft experiments were performed to confirm the in-vitro results.RESULTS MOB3B expression was reduced in CRC vs normal tissues and loss of MOB3B expression was associated with poor CRC prognosis.Overexpression of MOB3B protein in vitro attenuated the cell viability as well as the migration and invasion capacities of CRC cells,whereas knockdown of MOB3B expression had the opposite effects in CRC cells.At the molecular level,microtubule-associated protein light chain 3 II/I expression was elevated,whereas the expression of matrix metalloproteinase(MMP)2,MMP9,sequestosome 1,and phosphorylated mechanistic target of rapamycin kinase(mTOR)was downregulated in MOB3B-overexpressing RKO cells.In contrast,the opposite results were observed in tumor cells with MOB3B knockdown.The nude mouse data confirmed these in-vitro findings,i.e.,MOB3B expression suppressed CRC cell xenograft growth,whereas knockdown of MOB3B expression promoted the growth of CRC cell xenografts.CONCLUSION Loss of MOB3B expression promotes CRC development and malignant behaviors,suggesting a potential tumor suppressive role of MOB3B in CRC by inhibition of mTOR/autophagy signaling.
基金Supported by the National Natural Science Foundation of China,No.82260579the Natural Science Foundation of Guangxi,China,No.2020GXNSFAA159056the Natural Science Foundation Fostering Science Foundation of the Second Affiliated Hospital of Guangxi Medical University,Guangxi,China,No.GJPY2018010.
文摘Colorectal cancer(CRC)is a common malignancy that has the second highest incidence and mortality rate.Although there are many personalized treatment options for CRC,the therapeutic effects are ultimately limited by drug resistance.Studies have aimed to block the initiation and progression of CRC by inducing cell death to overcome this obstacle.Substantial evidence has indicated that both autophagy and ferroptosis play important regulatory roles in CRC.Autophagy,a lysosome-dependent process by which cellular proteins and organelles are degraded,is the basic mechanism for maintaining cell homeostasis.The duality and complexity of autophagy in cancer therapy is a hot topic of discussion.Ferroptosis,a regulated cell death pathway,is associated with iron accumulationinduced lipid peroxidation.The activation of ferroptosis can suppress CRC proliferation,invasion and drug resistance.Furthermore,recent studies have suggested an interaction between autophagy and ferroptosis.Autophagy can selectively degrade certain cellular contents to provide raw materials for ferroptosis,ultimately achieving antitumor and anti-drug resistance.Therefore,exploring the interaction between autophagy and ferroptosis could reveal novel ideas for the treatment of CRC.In this review,we describe the mechanisms of autophagy and ferroptosis,focusing on their roles in CRC and the crosstalk between them.
文摘BACKGROUND Small intestinal cavernous hemangioma is a rare disease,especially in the ileum.It is difficult to accurately diagnose due to its hidden location and nonspecific clinical symptoms.Here,we reported a case of ileal cavernous hemangioma with chronic hemorrhage in a 20-year-old man and review the literature to gain a better understanding of this disease.CASE SUMMARY The patient complained of intermittent melena and hematochezia for > 3 mo.The lowest hemoglobin level revealed by laboratory testing was 3.4 g/d L(normal range:12-16 g/dL).However,the gastroscopy,colonoscopy and peroral doubleballoon enteroscopy(DBE) showed no signs of bleeding.The transanal DBE detected a lesion at about 340 cm proximal to the ileocecal valve.Thus,we performed an exploratory laparoscopy and the lesion was resected.After the operation,the patient had no melena.Finally,the pathological examination identified the neoplasm as an ileal cavernous hemangioma,thereby resulting in gastrointestinal hemorrhage.CONCLUSION This report might improve the diagnosis and treatment of ileal cavernous hemangioma.
