Muhan Lü
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Muhan Lü has a total of 64 co-authors. Here are the top co-authors by number of shared publications:
- Hongjuan Cui
Medical Research Institute, State Key Laboratory of Resource Insects, Southwest University, Chongqing 400715, China
3 shared publications Feng Wang
State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400716, China
2 shared publicationsMingming Deng
The Affiliated Hospital of Southwest Medical University, Luzhou, China
2 shared publicationsQing Hu
Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, No. 25, Taiping Street, Jiangyang District, Luzhou, 64600, Sichuan, China
2 shared publicationsXi Zhou
Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, No. 25, Taiping Street, Jiangyang District, Luzhou, 64600, Sichuan, China
2 shared publicationsXiaomei Huang
Southwest Medical University, Zhongshan Street, Jiangyang District, Luzhou, 64600, Sichuan, China
2 shared publications
Latest Publications
- 24 April 2025
- Published by Elsevier in Phytomedicine
- Vol. 142, 156789
Mori Folium ethanol extracts induce ferroptosis and suppress gastric cancer progression by inhibiting the AKT/GSK3β/NRF2 axis
- 24 April 2025
- Published by Elsevier in Phytomedicine
- Vol. 142, 156789
Mori Folium ethanol extracts induce ferroptosis and suppress gastric cancer progression by inhibiting the AKT/GSK3β/NRF2 axis
- Open Access
- 1 November 2023
- Published by KEAI Publishing in Genes & Diseases
- Vol. 10 (6) , 2622-2638
PRMT1 promotes the proliferation and metastasis of gastric cancer cells by recruiting MLXIP for the transcriptional activation of the β-catenin pathway
Protein arginine methyltransferase 1 (PRMT1), a type I PRMT, is overexpressed in gastric cancer (GC) cells. To elucidate the function of PRMT1 in GC, PRMT1 expression in HGC-27 and MKN-45 cells was knocked down by short hairpin RNA (shRNA) or inhibited by PRMT1 inhibitors (AMI-1 or DCLX069), which resulted in inhibition of GC cell proliferation, migration, invasion, and tumorigenesis in vitro and in vivo. MLX-interacting protein (MLXIP) and Kinectin 1 (KTN1) were identified as PRMT1-binding proteins. PRMT1 recruited MLXIP to the promoter of β-catenin, which induced β-catenin transcription and activated the β-catenin signaling pathway, promoting GC cell migration and metastasis. Furthermore, KTN1 inhibited the K48-linked ubiquitination of PRMT1 by decreasing the interaction between TRIM48 and PRMT1. Collectively, our findings reveal a mechanism by which PRMT1 promotes cell proliferation and metastasis mediated by the β-catenin signaling pathway.
- 1 November 2023
- Published by KEAI Publishing in Genes & Diseases
- Vol. 10 (6) , 2622-2638
Open AccessPRMT1 promotes the proliferation and metastasis of gastric cancer cells by recruiting MLXIP for the transcriptional activation of the β-catenin pathway
Protein arginine methyltransferase 1 (PRMT1), a type I PRMT, is overexpressed in gastric cancer (GC) cells. To elucidate the function of PRMT1 in GC, PRMT1 expression in HGC-27 and MKN-45 cells was knocked down by short hairpin RNA (shRNA) or inhibited by PRMT1 inhibitors (AMI-1 or DCLX069), which resulted in inhibition of GC cell proliferation, migration, invasion, and tumorigenesis in vitro and in vivo. MLX-interacting protein (MLXIP) and Kinectin 1 (KTN1) were identified as PRMT1-binding proteins. PRMT1 recruited MLXIP to the promoter of β-catenin, which induced β-catenin transcription and activated the β-catenin signaling pathway, promoting GC cell migration and metastasis. Furthermore, KTN1 inhibited the K48-linked ubiquitination of PRMT1 by decreasing the interaction between TRIM48 and PRMT1. Collectively, our findings reveal a mechanism by which PRMT1 promotes cell proliferation and metastasis mediated by the β-catenin signaling pathway.
- Open Access
- 1 May 2023
- Published by KEAI Publishing in Genes & Diseases
- Vol. 10 (3) , 712-715
LncRNA MIR31HG controls the proliferation and metastasis of gastric cancer by c-CBL-mediated degradation of β-catenin
- 1 May 2023
- Published by KEAI Publishing in Genes & Diseases
- Vol. 10 (3) , 712-715
Open AccessLncRNA MIR31HG controls the proliferation and metastasis of gastric cancer by c-CBL-mediated degradation of β-catenin
- Open Access
- 30 June 2022
- Published by Wolters Kluwer Health in Medicine
- Vol. 101 (26) , e29770
The role of polyglycolic acid sheets in the management of post-endoscopic submucosal dissection gastrointestinal bleeding and esophageal stricture: A PRISMA compliant systematic review and meta-analysis
Background: As a relatively minimally invasive technique, endoscopic submucosal dissection (ESD) is widely used for the treatment of gastrointestinal lesions. However, it is associated with complications, such as postoperative bleeding, stricture, and perforation. A covering method using polyglycolic acid (PGA) sheets for ESD-induced ulcers has been reported to be effective in reducing the risk of post-ESD bleeding and esophageal stricture. Herein, we conducted a systematic review and meta-analysis to evaluate the role of PGA sheets in the prevention of gastrointestinal bleeding and esophageal stricture after ESD. Methods: We searched PubMed, Web of Science, and the Cochrane Library databases on October 15, 2019. All eligible articles were selected based on the predefined inclusion and exclusion criteria. The main outcomes were the rates of post-ESD gastrointestinal bleeding and esophageal stricture. Cochrane’s Q statistic and I2 test were used to identify heterogeneity between the studies. When there was no obvious heterogeneity (I2 < 50%, P > .1), a fixed-effect model was used. When there was obvious heterogeneity (I2 > 50%, P < .1), a random effect model was used. Funnel plots and the Egger regression test were used to assess publication bias. Results: Fifteen articles were included in the meta-analysis, of which 7 were exclusively about the use of PGA sheets to prevent postoperative gastrointestinal bleeding, and the remaining reported the use of PGA sheets to prevent postoperative esophageal stenosis. Our analysis showed that preventive therapy with PGA sheets decreased the rates of post-ESD gastrointestinal bleeding (risk ratio [RR] = 0.35, 95% confidential interval [CI]: 0.19–0.64, P < .001) and esophageal stricture (RR = 0.46, 95% CI: 0.27–0.79, P = .005), and the gastrointestinal bleeding and esophageal stricture rates after preventive treatment with PGA sheets were 5.7% (95% CI: 3.6%–8.8%) and 20.6% (95% CI: 14.5%–28.4%), respectively. Conclusion: The utilization of PGA sheets after ESD has an excellent outcome in reducing the risk of postoperative gastrointestinal bleeding and esophageal stricture.
- 30 June 2022
- Published by Wolters Kluwer Health in Medicine
- Vol. 101 (26) , e29770
Open AccessThe role of polyglycolic acid sheets in the management of post-endoscopic submucosal dissection gastrointestinal bleeding and esophageal stricture: A PRISMA compliant systematic review and meta-analysis
Background: As a relatively minimally invasive technique, endoscopic submucosal dissection (ESD) is widely used for the treatment of gastrointestinal lesions. However, it is associated with complications, such as postoperative bleeding, stricture, and perforation. A covering method using polyglycolic acid (PGA) sheets for ESD-induced ulcers has been reported to be effective in reducing the risk of post-ESD bleeding and esophageal stricture. Herein, we conducted a systematic review and meta-analysis to evaluate the role of PGA sheets in the prevention of gastrointestinal bleeding and esophageal stricture after ESD. Methods: We searched PubMed, Web of Science, and the Cochrane Library databases on October 15, 2019. All eligible articles were selected based on the predefined inclusion and exclusion criteria. The main outcomes were the rates of post-ESD gastrointestinal bleeding and esophageal stricture. Cochrane’s Q statistic and I2 test were used to identify heterogeneity between the studies. When there was no obvious heterogeneity (I2 < 50%, P > .1), a fixed-effect model was used. When there was obvious heterogeneity (I2 > 50%, P < .1), a random effect model was used. Funnel plots and the Egger regression test were used to assess publication bias. Results: Fifteen articles were included in the meta-analysis, of which 7 were exclusively about the use of PGA sheets to prevent postoperative gastrointestinal bleeding, and the remaining reported the use of PGA sheets to prevent postoperative esophageal stenosis. Our analysis showed that preventive therapy with PGA sheets decreased the rates of post-ESD gastrointestinal bleeding (risk ratio [RR] = 0.35, 95% confidential interval [CI]: 0.19–0.64, P < .001) and esophageal stricture (RR = 0.46, 95% CI: 0.27–0.79, P = .005), and the gastrointestinal bleeding and esophageal stricture rates after preventive treatment with PGA sheets were 5.7% (95% CI: 3.6%–8.8%) and 20.6% (95% CI: 14.5%–28.4%), respectively. Conclusion: The utilization of PGA sheets after ESD has an excellent outcome in reducing the risk of postoperative gastrointestinal bleeding and esophageal stricture.
- 3 October 2018
- Published by Springer Nature in Digestive Diseases and Sciences
- Vol. 64 (1) , 25-38
Research Progress on the Relationship Between Acute Pancreatitis and Calcium Overload in Acinar Cells
Acute pancreatitis is a human disease with multiple causes that leads to autodigestion of the pancreas. There is sufficient evidence to support the key role of sustained increase in cytosolic calcium concentrations in the early pathogenesis of the disease. To clarify the mechanism of maintaining calcium homeostasis in the cell and pathological processes caused by calcium overload would help to research directly targeted therapeutic agents. We will specifically review the following: intracellular calcium homeostasis and regulation, the occurrence of calcium overload in acinar cells, the role of calcium overload in the pathogenesis of AP, the treatment strategy proposed for calcium overload.
- 3 October 2018
- Published by Springer Nature in Digestive Diseases and Sciences
- Vol. 64 (1) , 25-38
Research Progress on the Relationship Between Acute Pancreatitis and Calcium Overload in Acinar Cells
Acute pancreatitis is a human disease with multiple causes that leads to autodigestion of the pancreas. There is sufficient evidence to support the key role of sustained increase in cytosolic calcium concentrations in the early pathogenesis of the disease. To clarify the mechanism of maintaining calcium homeostasis in the cell and pathological processes caused by calcium overload would help to research directly targeted therapeutic agents. We will specifically review the following: intracellular calcium homeostasis and regulation, the occurrence of calcium overload in acinar cells, the role of calcium overload in the pathogenesis of AP, the treatment strategy proposed for calcium overload.
- 23 March 2018
- Published by Wiley in Journal of Gastroenterology and Hepatology
- Vol. 33 (7) , 1365-1369
Use of an abdominal obstetric binder in colonoscopy: A randomized, prospective trial
Background and Aims: Various methods have been reported as aids to cecal intubation. This study aimed to prospectively investigate whether an abdominal obstetric binder (AOB) used during pregnancy and attached to the patients' abdomen during colonoscopy could facilitate effective colonoscopic insertion.Methods: This was a prospective study of 451 consecutive outpatient colonoscopies performed by a single experienced endoscopist. The recruited patients were randomly separated into two groups that received colonoscopy either with (Group A) or without an AOB attached (Group B). The cecal intubation time, cecal intubation length of the colonoscope, use of manual pressure, position change of each patient, and the number of patients with abdominal distension were collected for comparison.Results: A total of 451 patients (224 in Group A and 227 in Group B) were ultimately included in this study. In Group A, cecal intubation time and cecal intubation length of colonoscope (CIL) were significantly reduced (P < 0.001). The patients had significantly fewer position changes and manual pressure in Group A (P < 0.001). Significantly less abdominal distension was reported by patients in Group A (P < 0.001).Conclusions: During colonoscopy, the application of an AOB provided a significantly faster and more effective colonoscope insertion.
- 23 March 2018
- Published by Wiley in Journal of Gastroenterology and Hepatology
- Vol. 33 (7) , 1365-1369
Use of an abdominal obstetric binder in colonoscopy: A randomized, prospective trial
Background and Aims: Various methods have been reported as aids to cecal intubation. This study aimed to prospectively investigate whether an abdominal obstetric binder (AOB) used during pregnancy and attached to the patients' abdomen during colonoscopy could facilitate effective colonoscopic insertion.Methods: This was a prospective study of 451 consecutive outpatient colonoscopies performed by a single experienced endoscopist. The recruited patients were randomly separated into two groups that received colonoscopy either with (Group A) or without an AOB attached (Group B). The cecal intubation time, cecal intubation length of the colonoscope, use of manual pressure, position change of each patient, and the number of patients with abdominal distension were collected for comparison.Results: A total of 451 patients (224 in Group A and 227 in Group B) were ultimately included in this study. In Group A, cecal intubation time and cecal intubation length of colonoscope (CIL) were significantly reduced (P < 0.001). The patients had significantly fewer position changes and manual pressure in Group A (P < 0.001). Significantly less abdominal distension was reported by patients in Group A (P < 0.001).Conclusions: During colonoscopy, the application of an AOB provided a significantly faster and more effective colonoscope insertion.
- 1 January 2018
- Published by Elsevier in Cancer Letters
- Vol. 413, 94-101
Advances in esophageal cancer: A new perspective on pathogenesis associated with long non-coding RNAs
- 1 January 2018
- Published by Elsevier in Cancer Letters
- Vol. 413, 94-101
Advances in esophageal cancer: A new perspective on pathogenesis associated with long non-coding RNAs
- Open Access
- 31 August 2017
- Published by Korean Society for Parasitology in The Korean Journal of Parasitology
- Vol. 55 (4) , 391-398
Hookworm Infection: A Neglected Cause of Overt Obscure Gastrointestinal Bleeding
Hookworm infections are widely prevalent in tropical and subtropical areas, especially in low income regions. In the body, hookworms parasitize the proximal small intestine, leading to chronic intestinal hemorrhage and iron deficiency anemia. Occasionally, hookworms can cause overt gastrointestinal bleeding, but this is often ignored in heavily burdened individuals from endemic infectious areas. A total of 424 patients with overt obscure gastrointestinal bleeding were diagnosed by numerous blood tests or stool examinations as well as esophagogastroduodenoscopy, colonoscopy, capsule endoscopy or double-balloon enteroscopy. All of the patients lived in hookworm endemic areas and were not screened for hookworm infection using sensitive tests before the final diagnosis. The patients recovered after albendazole treatment, blood transfusion, and iron replacement, and none of the patients experienced recurrent bleeding in the follow-up. All the 31 patients were diagnosed with hookworm infections without other concomitant bleeding lesions, a rate of 7.3% (31/424). Seventeen out of 227 patients were diagnosed with hookworm infections in the capsule endoscopy (CE), and 14 out of 197 patients were diagnosed with hookworm infections in the double balloon enteroscopy (DBE). Hookworm infections can cause overt gastrointestinal bleeding and should be screened in patients with overt obscure gastrointestinal bleeding (OGIB) in endemic infectious areas with sensitive methods. Specifically, the examination of stool specimens is clinically warranted for most patients, and the proper examination for stool eggs relies on staff's communication.
- 31 August 2017
- Published by Korean Society for Parasitology in The Korean Journal of Parasitology
- Vol. 55 (4) , 391-398
Open AccessHookworm Infection: A Neglected Cause of Overt Obscure Gastrointestinal Bleeding
Hookworm infections are widely prevalent in tropical and subtropical areas, especially in low income regions. In the body, hookworms parasitize the proximal small intestine, leading to chronic intestinal hemorrhage and iron deficiency anemia. Occasionally, hookworms can cause overt gastrointestinal bleeding, but this is often ignored in heavily burdened individuals from endemic infectious areas. A total of 424 patients with overt obscure gastrointestinal bleeding were diagnosed by numerous blood tests or stool examinations as well as esophagogastroduodenoscopy, colonoscopy, capsule endoscopy or double-balloon enteroscopy. All of the patients lived in hookworm endemic areas and were not screened for hookworm infection using sensitive tests before the final diagnosis. The patients recovered after albendazole treatment, blood transfusion, and iron replacement, and none of the patients experienced recurrent bleeding in the follow-up. All the 31 patients were diagnosed with hookworm infections without other concomitant bleeding lesions, a rate of 7.3% (31/424). Seventeen out of 227 patients were diagnosed with hookworm infections in the capsule endoscopy (CE), and 14 out of 197 patients were diagnosed with hookworm infections in the double balloon enteroscopy (DBE). Hookworm infections can cause overt gastrointestinal bleeding and should be screened in patients with overt obscure gastrointestinal bleeding (OGIB) in endemic infectious areas with sensitive methods. Specifically, the examination of stool specimens is clinically warranted for most patients, and the proper examination for stool eggs relies on staff's communication.