BAIAP2L2 promotes the proliferation, migration and invasion of osteosarcoma associated with the Wnt/β-catenin pathway

Guo, Hong-Ting; Peng, Jing; Hu, Juan; Chang, Shi-Chuan; Liu, Huawen; Luo, Hao; Chen, Xiaohua; Tang, Haiping; Chen, Youhao

doi:10.1016/j.jbo.2021.100393

Cited by 12 publications

(9 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As reported, miR-98-5p is negatively mediated by SNHG4 in LC (Tang et al, 2019). Additionally, a report has illuminated that miR-98-5p expression is reduced in OC, and its silencing is available to alleviate OC cell development with cisplatin resistance (Guo et al, 2021).…”

Section: Discussionmentioning

confidence: 79%

“…Some factors like late diagnosis, chemotherapy resistance rate and easy recurrence lead to unpleasing prognosis and high mortality rate in OC patients (Wu et al, 2021). Novel evidence has illuminated that targeting aberrantly-expressed lncRNAs in OC may be latent biomarkers and curative targets for OC (Guo et al, 2021). Additionally, the lncRNA-microRNA-mRNA regulatory network offers novel perspective for brand-new therapy strategies for OC (Lin et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Promoting action of long non-coding RNA small nucleolar RNA host gene 4 in ovarian cancer

Liu¹,

Zhao

2023

Acta Biochim Pol

View full text Add to dashboard Cite

Objective: Long non-coding RNA (LncRNA) small nucleolar RNA host gene 4 (SNHG4) has been shown to be aberrantly expressed in a variety of cancers and involved in cancer development, but its role in ovarian cancer (OC) is unclear. The purpose of this study was to explore the biological function of SNHG4 in OC and reveal its potential downstream molecular targets. Methods: OC tumor tissue and normal tissue were collected; normal human ovarian epithelial cell line (IOSE80) and human ovarian cancer cell line (A2780, SKOV-3, OV-90 and CAOV3) were selected. RT-qPCR was used to detect SNHG4, miR-98-5p, and TMED5, while western blot was used to detect the protein expression levels of TMED5, Ki67, MMP-9, Bcl-2, Bax, Gsk3β, Wnt3a, and β-catenin. The subcellular localization of SNHG4 was assessed by nucleocytoplasmic separation assay. CCK-8, colony formation assay, flow cytometry, and Transwell were used to assess the biological behavior of OC cells. The targeting relationship between SNHG4, miR-98-5p and TMED5 was verified by dual luciferase reporter assay and RIP assay. Results: In OC, SNHG4 and TMED5 were highly expressed, and miR-98-5p was underexpressed. Knockdown of SNHG4 inhibited OC cell proliferation, migration and invasion, promoted apoptosis, and prevented Wnt/β-catenin pathway activation. The effect of knockdown of SNHG4 was reversed by knockdown of miR-98-5p or overexpression of TMED5. Mechanistically, SNHG4 competitively adsorbed miR-98-5p to mediate TMED5 expression, thereby activating the Wnt/β-catenin pathway. Conclusion: SNHG4 accelerates OC development via mediating the miR-98-5p/TMED5 axis and activating the Wnt/β-Catenin pathway. SNHG4 gene silencing might be a novel option for OC treatment.

show abstract

Section: Discussionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Promoting action of long non-coding RNA small nucleolar RNA host gene 4 in ovarian cancer

Liu¹,

Zhao

2023

Acta Biochim Pol

View full text Add to dashboard Cite

show abstract

“…Trophinin-associated protein (TROAP) has been reported to be highly expressed and promotes tumour progression in HCC [ 40 ], prostate cancer [ 41 ], breast cancer [ 42 ], glioma [ 43 ], gastric cancer [ 44 ], and clear cell renal cell carcinoma [ 45 ]. BAIAP2L2 [ 46 , 47 ], pituitary tumour-transforming gene 1 (PTTG1) [ 48 , 49 ] and complement factor H-related 3 (CFHR3) [ 50 ] have also been reported to be overexpressed in many types of human cancer and to promote tumour cell angiogenesis, migration and invasion. However, the advantage of our study was that the expression levels of these gene were assessed in large samples of HCC tissues.…”

Section: Discussionmentioning

confidence: 99%

Prediction of hepatocellular carcinoma prognosis and immunotherapeutic effects based on tryptophan metabolism-related genes

Xue

Zhao

et al. 2022

Cancer Cell Int

View full text Add to dashboard Cite

Background L-tryptophan (Trp) metabolism involved in mediating tumour development and immune suppression. However, comprehensive analysis of the role of the Trp metabolism pathway is still a challenge. Methods We downloaded Trp metabolism-related genes’ expression data from different public databases, including TCGA, Gene Expression Omnibus (GEO) and Hepatocellular Carcinoma Database (HCCDB). And we identified two metabolic phenotypes using the ConsensusClusterPlus package. Univariate regression analysis and lasso Cox regression analysis were used to establish a risk model. CIBERSORT and Tracking of Indels by DEcomposition (TIDE) analyses were adopted to assess the infiltration abundance of immune cells and tumour immune escape. Results We identified two metabolic phenotypes, and patients in Cluster 2 (C2) had a better prognosis than those in Cluster 1 (C1). The distribution of clinical features between the metabolic phenotypes showed that patients in C1 tended to have higher T stage, stage, grade, and death probability than those of patients in C2. Additionally, we screened 739 differentially expressed genes (DEGs) between the C1 and C2. We generated a ten-gene risk model based on the DEGs, and the area under the curve (AUC) values of the risk model for predicting overall survival. Patients in the low-risk subgroup tended to have a significantly longer overall survival than that of those in the high-risk group. Moreover, univariate analysis indicated that the risk model was significantly correlated with overall survival. Multivariate analysis showed that the risk model remained an independent risk factor in hepatocellular carcinoma (p < 0.0001). Conclusions We identified two metabolic phenotypes based on genes of the Trp metabolism pathway, and we established a risk model that could be used for predicting prognosis and guiding immunotherapy in patients with hepatocellular carcinoma.

show abstract

“…To evaluate the in vivo anticancer action of caudatin, mice (4-6 weeks old immunodefcient Balb/C nude mice, Shanghai, China) were injected with MG63 cells (5 × 106) to establish xenograft tumorigenesis model, according to the published report [13]. 2 weeks after cell injection, mice (n � 12) were randomly divided into sham (intraperitoneal injection with PBS) and caudatin (intraperitoneal injection with 50 mg/kg every 2…”

Section: Xenograft Tumorigenesis In Nude Micementioning

confidence: 99%

Caudatin Inhibits the Proliferation, Invasion, and Glycolysis of Osteosarcoma Cells via the Wnt/β- Catenin Pathway

Zhang

Sheng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Background. Caudatin is a steroidal glycoside with reported anticancer activity in a variety of studies. Nevertheless, the role and mechanisms of caudatin in osteosarcoma (OS) remain unclear. In this study, we explored the potential anticancer effects of caudatin in OS cells and investigated the underlying mechanisms. Methods. Both the CCK8 proliferation assay and flow cytometry were employed to evaluate cell proliferation and apoptosis. A transwell assay was applied to determine cell invasion ability. Besides, glycolytic capacity was examined by measuring glucose consumption, lactic acid production, as well as ATP production. A western blot was utilized to assess the protein levels of β-catenin, CyclinD 1, C-myc, HK2 (Hexokinase 2), LDHA (lactate dehydrogenase), as well as epithelial-mesenchymal transition (EMT)-related markers. The inhibitory effect of caudatin on tumor growth was investigated using a xenograft tumorigenesis model. Results. Caudatin restrained cellular glycolysis, suppressed cell proliferation and invasion by reducing HK2 and LDHA expression and regulating the Wnt/β-Catenin signaling pathway. Caudatin treatment caused the upregulation of E-cadherin and suppressed N-cadherin expression. Further, caudatin treatment impaired cell viability, invasion ability, and intracellular glycolysis level but induced apoptosis. The administration of BML 284 reversed the inhibitory effects of caudatin. Moreover, caudatin suppressed the tumorigenesis of OS cells in the xenograft model of nude mice. Conclusions. Our study revealed the anticancer effects of caudatin, including proliferation inhibition, cell invasion suppression, and glycolysis impairment. These effects seem to be executed through targeting the Wnt/β-Catenin signaling pathway. These data indicate that caudatin may be formulated as a potential therapeutic for osteosarcoma.

show abstract

BAIAP2L2 promotes the proliferation, migration and invasion of osteosarcoma associated with the Wnt/β-catenin pathway

Abstract: Highlights BAIAP2L2 participated in the development of human osteosarcoma. BAI1 activity was altered during the development, proliferation and apoptosis of tumor cells. Expression of BAIAP2L2 and Ki67 was greatly down-regulated by knockdown of BAIAP2L2.

Cited by 12 publications

References 27 publications

Promoting action of long non-coding RNA small nucleolar RNA host gene 4 in ovarian cancer

Promoting action of long non-coding RNA small nucleolar RNA host gene 4 in ovarian cancer

Prediction of hepatocellular carcinoma prognosis and immunotherapeutic effects based on tryptophan metabolism-related genes

Caudatin Inhibits the Proliferation, Invasion, and Glycolysis of Osteosarcoma Cells via the Wnt/β- Catenin Pathway

Contact Info

Product

Resources

About