Downregulation of CRABP2 Inhibit the Tumorigenesis of Hepatocellular Carcinoma In Vivo and In Vitro

Chen, Qingmin; Tan, Ludong; Jin, Zhe; Liu, Yahui; Zhang, Ze

doi:10.1155/2020/3098327

Cited by 18 publications

(15 citation statements)

References 41 publications

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“…Overexpression of CRABP2 activated phosphorylation of PI3K/Akt signaling pathway. Chen et al [ 16 ] revealed that CRABP2 knockdown suppressed tumor growth in nude mice xenografts.…”

Section: Discussionmentioning

confidence: 99%

“…Wu et al [ 15 ] found that CRABP2 promotes metastasis of lung cancer cells via HuR and Integrin β1/FAK/ERK signaling pathway. Chen et al [ 16 ] revealed that downregulation of CRABP2 inhibit the tumorigenesis of hepatocellular carcinoma in vivo and in vitro. However, the role of CRABP2 in regulating dexamethasone induced osteoblast apoptosis and ONFH was unknown.…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of CRABP2 inhibits dexamethasone-induced apoptosis in human osteoblast cells

Zhang

Sun

et al. 2021

J Orthop Surg Res

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Background The purpose of the current study was to explore the role and underlying mechanism of cellular retinoic acid binding protein 2 (CRABP2) in dexamethasone (DEX)-induced apoptosis in human osteoblast cells. Methods GSE10311 was downloaded from the Gene Expression Omnibus (GEO) database to identify the differentially expressed genes (DEGs) by the limma/R package. Primary human osteoblast was isolated and treated with different concentration of DEX (0, 10-8, 10-7, 10-6, 10-5, and 10-4 mol/L), and cell viability and flow cytometry were used to detect cell proliferation and apoptosis. A CRABP2 overexpression plasmid (oe-CRABP2) was used to overexpress CRABP2, and western blotting was conducted to detect protein expression. Results We found that CRABP2 was downregulated in the DEX-treated group. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses indicated that DEGs were associated with PI3K/Akt signaling pathway. DEX downregulated CRABP2 gene and protein expression, inhibited viability, and induced human osteoblast apoptosis. Overexpression of CRABP2 reversed DEX-induced apoptosis in human osteoblast. Moreover, overexpression of CRABP2 delayed the progression of DEX-induced osteonecrosis of the femoral head (ONFH) animal model. Conclusion In conclusion, CRABP2 is effective at inhibiting DEX-induced human osteoblast apoptosis and delayed ONFH progression.

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“…Overexpression of CRABP2 activated phosphorylation of PI3K/Akt signaling pathway. Chen et al [ 16 ] revealed that CRABP2 knockdown suppressed tumor growth in nude mice xenografts.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Overexpression of CRABP2 inhibits dexamethasone-induced apoptosis in human osteoblast cells

Zhang

Sun

et al. 2021

J Orthop Surg Res

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“…S100a4 is an epithelial-mesenchymal transition mediator associated with the maintenance of cancer-initiating cells in HNSCC 20 . Aberrant expression of Crabp2 is correlated with oncogenesis in lung and liver cancers 21 , 22 . Id3, often in concert with Id1, is essential for the self-renewal of tumor-initiating cells in several malignancies including glioma, breast cancer, and colon cancer 23 – 25 .…”

Section: Discussionmentioning

confidence: 99%

Characterization of normal and cancer stem-like cell populations in murine lingual epithelial organoids using single-cell RNA sequencing

Johansson

Ueno

2021

Sci Rep

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The advances in oral cancer research and therapies have not improved the prognosis of patients with tongue cancer. The poor treatment response of tongue cancer may be attributed to the presence of heterogeneous tumor cells exhibiting stem cell characteristics. Therefore, there is a need to develop effective molecular-targeted therapies based on the specific gene expression profiles of these cancer stem-like cell populations. In this study, the characteristics of normal and cancerous organoids, which are convenient tools for screening anti-cancer drugs, were analyzed comparatively. As organoids are generally generated by single progenitors, they enable the exclusion of normal cell contamination from the analyses. Single-cell RNA sequencing analysis revealed that p53 signaling activation and negative regulation of cell cycle were enriched characteristics in normal stem-like cells whereas hypoxia-related pathways, such as HIF-1 signaling and glycolysis, were upregulated in cancer stem-like cells. The findings of this study improved our understanding of the common features of heterogeneous cell populations with stem cell properties in tongue cancers, that are different from those of normal stem cell populations; this will enable the development of novel molecular-targeted therapies for tongue cancer.

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“…Due to the lack of early screening and detection techniques, most of the patients are diagnosed at an advanced stage. Currently, the mainstream treatments for HCC are surgical resection and liver transplantation (Hsueh et al, 2016); however, the 5‐year recurrence rate of HCC is more than 60%, contributing to a poor prognosis and survival rate (Chen et al, 2020). Hence, it is imminently required to seek for new therapies for HCC.…”

Section: Introductionmentioning

confidence: 99%

Combination of canstatin and arsenic trioxide suppresses the development of hepatocellular carcinoma

Zhang

Duan

Song

et al. 2020

Drug Development Research

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Complication of arsenic trioxide (ATO) and other drugs in cancer treatment has attracted much focus, but is limitedly investigated in hepatocellular carcinoma (HCC). This study aimed to explore the role of ATO combined with canstatin in HCC. HepG2 cells were treated with different concentrations of ATO with or without canstatin, CCK‐8, flow cytometry, Transwell assays were conducted to determine cell proliferation, apoptosis, adhesion, migration, and invasion abilities. Besides, the protein expression or mRNA level of caspase‐3, PCNA, and MMP‐2 was measured using western blotting or qRT‐PCR. BALB/c‐nu/nu mice were used to establish nude mouse transplantation tumor model, and received ATO or canstatin treatment for 3 weeks. The results showed that ATO inhibited cell proliferation, adhesion, migration and invasion, and promoted cell apoptosis with a concentration‐dependent way. Canstatin had a significantly inhibitory effect on cell proliferation, but had limited effects on the other cellular behaviors. Besides, combination with ATO and canstatin strengthened the effects of ATO alone on cell proliferation inhibition and cell apoptosis promotion. Moreover, both of ATO and canstatin increased the protein expression of caspase‐3, while decreased PCNA and MMP‐2, which was further strengthened upon their combination. Furthermore, both of ATO and canstatin inhibited tumor growth in vivo, which was also strengthened upon their combination. Collectively, we found that combined canstatin and ATO significantly inhibited cell proliferation, migration and adhesion abilities, and promoted cell apoptosis, and inhibited tumor growth, thus suppressed the progression of HCC.

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Downregulation of CRABP2 Inhibit the Tumorigenesis of Hepatocellular Carcinoma In Vivo and In Vitro

Cited by 18 publications

References 41 publications

Overexpression of CRABP2 inhibits dexamethasone-induced apoptosis in human osteoblast cells

Overexpression of CRABP2 inhibits dexamethasone-induced apoptosis in human osteoblast cells

Characterization of normal and cancer stem-like cell populations in murine lingual epithelial organoids using single-cell RNA sequencing

Combination of canstatin and arsenic trioxide suppresses the development of hepatocellular carcinoma

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