Rap2B promotes angiogenesis via PI3K/AKT/VEGF signaling pathway in human renal cell carcinoma

Di, Jiehui; Gao, Keyu; Qu, Debao; Yang, Jing; Zheng, Junnian

doi:10.1177/1010428317701653

Cited by 25 publications

(20 citation statements)

References 41 publications

(53 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This pathway is a promising drug target. 33 – 37 In this research, we found that silencing CAV2 inhibited the expression of EGFR, PI3K and p-AKT in vitro and in vivo. We also found that the expression of CAV2 was positively correlated with EGFR, PI3K and AKT.…”

Section: Discussionmentioning

confidence: 67%

CAV2 promotes the growth of renal cell carcinoma through the EGFR/PI3K/Akt pathway

Shangli

Hu³

2018

OTT

View full text Add to dashboard Cite

BackgroundCaveolin-2 (CAV2) is reported to have an important role in cancer. The following study investigated the expression and function of CAV2 in kidney cancer in vitro and in vivo.Materials and methodsReal-time PCR, immunohistochemistry and Western blotting analysis were used to determine CAV2, epidermal growth factor receptor (EGFR), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) in kidney cancer cell line OS-RC-2 and clinical specimens. The role of CAV2 in maintaining kidney cancer malignant phenotype was examined by wound healing assay, Matrigel invasion assays and mouse orthotopic xenograft model.ResultsHigher expression of CAV2 was found in renal cell carcinoma tissue compared to normal tissue. Furthermore, increased expression of CAV2 was associated with cancer progression. Also, silencing of CAV2 inhibited the proliferation, migration and invasion, as well as the expression of EGFR, PI3K and p-Akt in OS-RC-2 cells in vitro, and OS-RC-2 xenograft growth in vivo.ConclusionOur results revealed that CAV2 promotes the growth of renal cell carcinoma through EGFR/PI3K/Akt pathway.

show abstract

Section: Discussionmentioning

confidence: 67%

CAV2 promotes the growth of renal cell carcinoma through the EGFR/PI3K/Akt pathway

Shangli

Hu³

2018

OTT

View full text Add to dashboard Cite

show abstract

“…MiR-105 acts as a tumor suppressor or an oncogene, depending on the particular tumor context and base-pairing genes. RAP2B , a member of the GTP-binding proteins, is generally increased in many types of tumors such as glioma 23 , colorectal cancer 24 , and renal cell carcinoma 19 . We predicted that RAP2B may be a potential target of miR-105 by bioinformatics analysis ( http://www.targetscan.org/ ).…”

Section: Discussionmentioning

confidence: 99%

“…The RAP2B gene belongs to the RAS oncogene superfamily. Current research on RAP2B shows that it mainly plays a role as a cancer-promoting factor in a variety of diseases, and plays an important role in the migration and invasion of tumor cells such as lung cancer 18 , renal cell carcinoma 19 , and prostate cancer 20 .…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA GHET1/miR-105/RAP2B axis regulates the progression of acute myeloid leukemia

Xiao¹,

Li²,

Xue³

et al. 2020

J. Cancer

View full text Add to dashboard Cite

Background: To explore the biological effects and potential molecular mechanisms of long non-coding RNA (lncRNA) gastric carcinoma proliferation enhancing transcript 1 (GHET1) in acute myeloid leukemia (AML). Methods: Fluorescence in situ hybridization was performed to determine the location of GHET1. Quantitative polymerase chain reaction (qPCR) was performed to verify RNA expression. GHET1 overexpression and knockdown were achieved by transfection of the expression vector or short hairpin RNA. Western blotting, qPCR, Cell Counting Kit-8 assay, JC-1 staining, and flow cytometry were performed to measure GHET1 function. The dual luciferase reporter assay was performed to confirm the relationship between microRNA 105 (mir-105) and Ras-related protein Rap-2B ( RAP2B ). Results: GHET1 was localized in the nucleus of NB4 cell lines. GHET1 expression was elevated in AML cell lines compared with normal bone marrow mononuclear cells. GHET1 knockdown led to inhibition of proliferation and promoted the differentiation and apoptosis of AML cell lines. Furthermore, GHET1 directly bound to miR-105 and downregulated miR-105 expression. MiR-105 overexpression suppressed proliferation and induced the differentiation and apoptosis of AML cell lines. In addition, RAP2B was confirmed to be a target gene of miR-105 and an inverse correlation was shown between their expression levels in AML cell lines; when miR-105 increased, Rap-2B level decreased and vice versa . Conclusion: This study demonstrated that the GHET1/miR-105/ Rap2B axis may be a critical signaling pathway involved in AML progression.

show abstract

“…Activation of the PI3K/AKT/mTOR signaling pathway directly regulates specific gene expression by affecting downstream protein kinases, such as apoptosis-associated cellular molecules, including caspase-3, caspase-9, Bcl-2 and Bax, cell cycle-associated factors, including cyclin D1 and E, and by participating in the regulation of cell proliferation and apoptosis (47,48). In addition, activation of the PI3K/AKT signaling pathway promotes VEGF synthesis (49) and VEGF binds to its receptor to feedback activation of PI3K. Activation of PI3K/AKT and VEGF further promote MMP expression and mediate tumor cell infiltration and metastasis (50).…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB‑152 in�vivo and in�vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

Teng¹,

Xu²,

Qin³

2019

Oncol Rep

View full text Add to dashboard Cite

Acute lymphoblastic leukemia (ALL) is a malignant hematological disease. Tanshinone IIA (Tan IIA) has antitumor activity in vitro and in vivo. The aim of the present study was to investigate the effects of Tan IIA in combination with imatinib (IM) on the proliferation, apoptosis, migration and invasion of acute T lymphocytic leukemia TIB-152 cells in vivo and in vitro, and analyze the potential underlying mechanism. Tan IIA and IM, alone and in combination, significantly inhibited proliferation, migration and invasion of TIB-152 cells, and promoted apoptosis; the effect of co-treatment with Tan IIA plus IM was enhanced. IGF-1 promoted the proliferation, migration and invasion of TIB-152 cells and inhibited apoptosis, while Tan IIA treatment significantly reversed these effects. In vivo experiments demonstrated that treatment with Tan IIA and IM, alone or in combination, significantly inhibited tumor growth in TIB-152 xenograft mice; the growth inhibition of Tan IIA plus IM was the strongest observed. Western blot analysis revealed that the combination of Tan IIA and IM resulted in significantly lower levels of p-PI3K, p-AKT and p-mTOR in cells and tissues compared with the IM and Tan alone treatment groups. In addition, the combination of Tan IIA and IM significantly decreased the levels of Ki67, cleaved caspase-3, VEGF and MMP-9 in cells and tissues, and the level of caspase-3 was significantly increased. Taken together, the results revealed that Tan IIA enhanced the inhibitory effect of imatinib on TIB-152 cell proliferation, migration and invasion, and induced apoptosis, which may be associated with inhibition of the PI3K/AKT/mTOR signaling pathway. Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB-152 in vivo and in vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

show abstract

Rap2B promotes angiogenesis via PI3K/AKT/VEGF signaling pathway in human renal cell carcinoma

Cited by 25 publications

References 41 publications

CAV2 promotes the growth of renal cell carcinoma through the EGFR/PI3K/Akt pathway

CAV2 promotes the growth of renal cell carcinoma through the EGFR/PI3K/Akt pathway

Long non-coding RNA GHET1/miR-105/RAP2B axis regulates the progression of acute myeloid leukemia

Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB‑152 in�vivo and in�vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

Contact Info

Product

Resources

About