Oridonin Induces Apoptosis in Esophageal Squamous Cell Carcinoma by Inhibiting Cytoskeletal Protein LASP1 and PDLIM1

Zhang, Xiaojun; Xing, Mengtao; Ma, Yangcheng; Zhang, Zhuangli; Qiu, Cuipeng; Wang, Xiao; Zhao, Zhihong; Ji, Zhenyu; Zhang, Jianying

doi:10.3390/molecules28020805

Cited by 5 publications

(2 citation statements)

References 56 publications

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“…Based on previous studies [35,36], a total of eight patients (choledocholithiasis, n = 4; HCC, n = 4) were included in this study. Bile samples were mixed with pre-cooled acetone at a four-fold volume of precipitation.…”

Section: Two-dimensional Electrophoresis (2-de)mentioning

confidence: 99%

Silencing of peroxiredoxin 2 suppresses proliferation and Wnt/β-catenin pathway, and induces senescence in hepatocellular carcinoma

YANG,

XIANG,

et al. 2024

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Hepatocellular carcinoma (HCC), a common malignancy worldwide, still lacks effective clinical treatment. The study aimed to investigate the oncogenes that affect the progression of HCC and their possible mechanisms. In our study, we initially confirmed a higher level of PRDX2 in the bile of HCC patients compared to those with choledocholithiasis by 2-DE, LC-MS, and ELISA. Subsequently, we demonstrated the high expression of peroxiredoxin 2 (PRDX2) in HCC based on the TCGA database and clinical sample analysis. Furthermore, PRDX2 overexpression enhanced the viability of HCC cells. And PRDX2 silencing induced senescence of HCC cells. In vivo, knockdown of PRDX2 significantly reduced the weight of xenograft tumors. PRDX2 also was found to activate the Wnt/β-catenin pathway by inducing β-catenin nuclear translocation. Consequently, we proved that silencing PRDX2 could inhibit proliferation and Wnt/ β-catenin pathway while promoting senescence in HCC cells.

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Section: Two-dimensional Electrophoresis (2-de)mentioning

confidence: 99%

Silencing of peroxiredoxin 2 suppresses proliferation and Wnt/β-catenin pathway, and induces senescence in hepatocellular carcinoma

YANG,

XIANG,

et al. 2024

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show abstract

“…Interestingly, Oridonin might represent a potential agent inducing apoptosis of the CRC and human gastric cancer cisplatin-resistant SGC7901/DDP cells through ROS/JNK/c-Jun axis and Caspase activation, respectively [ 161 , 162 ]. Albeit the mechanistic link with NLRP3 pathway is still missing, by inhibiting cytoskeletal protein LASP1 and PDLIM1, Oridonin induces apoptosis of EC cells, thus arresting cancer growth [ 163 ]. Similarly, in pancreatic gemcitabine resistant cancer cell, the LRP1/ERK/JNK signaling is susceptible to Oridonin, which promotes apoptosis and overcomes drug resistance [ 164 ].…”

Section: Nlrp3 Targeted Pharmacological Interventions In Gi Cancersmentioning

confidence: 99%

The ‘speck’-tacular oversight of the NLRP3-pyroptosis pathway on gastrointestinal inflammatory diseases and tumorigenesis

Arrè,

Scialpi,

Centonze

et al. 2023

J Biomed Sci

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The NLRP3 inflammasome is an intracellular sensor and an essential component of the innate immune system involved in danger recognition. An important hallmark of inflammasome activation is the formation of a single supramolecular punctum, known as a speck, per cell, which is the site where the pro-inflammatory cytokines IL-1β and IL-18 are converted into their bioactive form. Speck also provides the platform for gasdermin D protein activation, whose N-terminus domain perforates the plasma membrane, allowing the release of mature cytokines alongside with a highly inflammatory form of cell death, namely pyroptosis. Although controlled NLRP3 inflammasome-pyroptosis pathway activation preserves mucosal immunity homeostasis and contributes to host defense, a prolonged trigger is deleterious and could lead, in genetically predisposed subjects, to the onset of inflammatory bowel disease, including Crohn's disease and ulcerative colitis, as well as to gastrointestinal cancer. Experimental evidence shows that the NLRP3 inflammasome has both protective and pathogenic abilities. In this review we highlight the impact of the NLRP3-pyroptosis axis on the pathophysiology of the gastrointestinal tract at molecular level, focusing on newly discovered features bearing pro- and anti-inflammatory and neoplastic activity, and on targeted therapies tested in preclinical and clinical trials.

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Induction of apoptosis by oridonin in nonfunctioning pituitary adenoma cells

Chen,

Yuan,

Wang

et al. 2024

Drug Development Research

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Nonfunctioning pituitary adenoma (NFPA) is one of the major subtypes of pituitary adenomas (PA) and its primary treatment is surgical resection. However, normal surgery fails to remove lesions completely and there remains in lack of frontline treatment, so the development of new drugs for NFPA is no doubt urgent. Oridonin (ORI) has been reported to have antitumor effects on a variety of tumors, but whether it could exhibit the same effect on NFPA requires to be further investigated. The effects of ORI on pituitary‐derived folliculostellate cell line (PDFS) cell viability, colony formation, proliferation ability, migration, and invasion were examined by Cell Counting Kit‐8, colony formation assay, 5‑Ethynyl‑2'‑deoxyuridine proliferation assay, wound‐healing assay, and Transwell assay. The differentially expressed genes in the control and ORI‐treated groups were screened by transcriptome sequencing analysis and analyzed by Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment. Cell cycle analysis was performed to detect changes in cell cycle. Annexin V‐fluorescein isothiocyanate/propidium iodide staining was performed to detect apoptosis in ORI‐treated cells. Western blot assay was performed to detect Bax, Bcl‐2, and cleaved Caspase‐3 protein expression. ORI inhibited PDFS cell viability and significantly suppressed cell proliferation, migration, and invasion. GO and KEGG results showed that ORI was associated with signaling pathways such as cell cycle and apoptosis in PDFS cells. In addition, ORI blocked cells in G2/M phase and induced apoptosis in PDFS cells. ORI can trigger cell cycle disruption and apoptosis collaboratively in PDFS cells, making it a promising and effective agent for NFPA therapy.

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Oridonin Induces Apoptosis in Esophageal Squamous Cell Carcinoma by Inhibiting Cytoskeletal Protein LASP1 and PDLIM1

Cited by 5 publications

References 56 publications

Silencing of peroxiredoxin 2 suppresses proliferation and Wnt/β-catenin pathway, and induces senescence in hepatocellular carcinoma

Silencing of peroxiredoxin 2 suppresses proliferation and Wnt/β-catenin pathway, and induces senescence in hepatocellular carcinoma

The ‘speck’-tacular oversight of the NLRP3-pyroptosis pathway on gastrointestinal inflammatory diseases and tumorigenesis

Induction of apoptosis by oridonin in nonfunctioning pituitary adenoma cells

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