Cellular retinol binding protein-1 inhibits cancer stemness via upregulating WIF1 to suppress Wnt/β-catenin pathway in hepatocellular carcinoma

Liu, Xiangye; Shan, Wenhua; Li, Tingting; Gao, Xiaoge; Kong, Fanyun; You, Hua; Kong, Delong; Qiao, Shuxi; Tang, Renxian

doi:10.1186/s12885-021-08967-2

Cited by 17 publications

(9 citation statements)

References 57 publications

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“…Besides, it was reported that RBP1 enhanced the malignancy of non-glioblastomatous diffuse gliomas through the activation of NF-κB signaling (Wu et al 2022). In contrast, RBP1 inhibits the Wnt/β-catenin pathway by upregulating WIF1 to reduce cancer stem cells, thus providing a new therapeutic target for the clinical treatment of liver cancer (Liu et al 2021). These ndings demonstrate that the function of RBP1 in diverse cancers is different.…”

Section: Discussionmentioning

confidence: 99%

RBP1 promotes the progression of eyelid basal cell carcinoma via regulating OGN expression

Chen

Wang

et al. 2023

Preprint

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Objective Using RBP1 as the core gene to investigate the effects of RBP1 on the proliferation, migration and invasion of eyelid BCC cell line A431, and to explore its role in a mouse xenograft tumor model. To study in depth the specific molecular mechanisms by which RBP1 promotes the malignant progression of eyelid BCC, RNA-seq as well as bioinformatics analysis was performed to search for downstream genes with the aim of providing new potential targets for the treatment of eyelid BCC. Methods A sample of 30 patients with eyelid BCC who underwent surgery in the ophthalmology department of Huai'an First Hospital of Nanjing Medical University was selected. Protein mass spectrometry was used to examine three of the pairs of eyelid BCC cancer tissues and paracancerous tissues, and RBP1 was found to be highly expressed in eyelid BCC. The effect of RBP1 on eyelid BCC was investigated by clinical sample validation, in vitro cytology and mouse xenograft tumor model, and the downstream gene osteoglycin (OGN) was further screened by RNA-seq technology to verify that RBP1 can be involved in eyelid BCC progression by regulating OGN levels. Results The results showed that RBP1 was significantly more expressed in eyelid BCC tissues than in paracancerous tissues, and cellular experiments confirmed that RBP1 promoted proliferation, migration and invasion of eyelid BCC cells, and a mouse xenograft tumor model revealed that the gene could promote the growth of cancerous species. Meanwhile, salvage experiments showed that RBP1 accelerated the proliferation, migration, invasion and tumor growth of eyelid BCC cells in nude mice by suppressing OGN protein levels. Conclusion RBP1 was significantly upregulated in eyelid BCC. Interfering with RBP1 not only inhibited the proliferation, migration and invasion of A431 cells, but also inhibited the growth of transplanted tumors in nude mice. In addition, knockdown of OGN reversed the inhibitory effects of RBP1 interference on cell proliferation, migration and invasion. In summary, RBP1 can promote tumor progression in eyelid BCC by inhibiting OGN expression, which provides a new potential target for the treatment of eyelid BCC.

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Section: Discussionmentioning

confidence: 99%

RBP1 promotes the progression of eyelid basal cell carcinoma via regulating OGN expression

Chen

Wang

et al. 2023

Preprint

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“…Fortunately, the role of the aforementioned pathways in the pathogenesis of HCC has been verified in in vitro experiments. Liu et al (2021b ) revealed that cellular retinol binding protein-1 inhibits cancer stemness via upregulating WIF1 to suppress the Wnt/β-catenin pathway in hepatocellular carcinoma. Meanwhile, Yassin et al (2022 ) explored silybum marianum total extract, silymarin and silibinin abate hepatocarcinogenesis, and hepatocellular carcinoma growth via modulation of the TNF signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Construction of a Necroptosis-Related miRNA Signature for Predicting the Prognosis of Patients With Hepatocellular Carcinoma

et al. 2022

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Background: Many miRNAs have been demonstrated to be associated with the prognosis of hepatocellular carcinoma (HCC). However, how to combine necroptosis-related miRNAs to achieve the best predictive effect in estimating HCC patient survival has not been explored.Methods: The mRNA and miRNA expression profile were downloaded from a public database (TCGA-LIHC cohort). Necroptosis-related genes were obtained from previous references, and necroptosis-related miRNAs were identified using Pearson analysis. Subsequently, differential expression miRNAs (DEms) were identified in HCC and paracancer normal samples based on necroptosis-related miRNA expression. The whole set with HCC was randomized into a training set and testing set (1:1). LASSO-Cox regression analysis was used to construct an miRNA signature. Multiple statistical methods were used to validate the clinical benefit of signature in HCC patients, including receiver operator characteristic (ROC) curves, Kaplan–Meier survival analyses, and decision curve analysis (DCA). The downstream target genes of miRNAs were obtained from different online tools, and the potential pathways involved in miRNAs were explored. Finally, we conducted RT-qPCR in SK-HEP-1, THLE-3, and HUH-7 cell lines for miRNAs involved in the signature.Results: The results showed that a total of eight specific necroptosis-related miRNAs were screened between HCC and adjacent tissues in the training set. Subsequently, based on the aforementioned miRNAs, 5-miRNA signature (miR-139-5p, hsa-miR-326, miR-10b-5p, miR-500a-3p, and miR-592) was generated by LASSO-Cox regression analysis. Multivariate Cox regression analysis showed that the risk scores were independent prognostic indicators in each set. The area under curves (AUCs) of 1 year, 3 years, 5 years, and 7 years were high in each set (AUC >0.7). DCA analysis also revealed that the risk score had a potential benefit than other clinical characteristics. Meanwhile, survival analysis showed that the high-risk group showed low survival probabilities. Moreover, the results of enrichment analysis showed that specific miRNAs were mainly enriched in the cAMP signaling pathway and TNF signaling pathway. Finally, the results of RT-qPCR were consistent with the prediction results in public databases.Conclusion: Our study establishes a robust tool based on 5-necroptosis-related miRNAs for the prognostic management of HCC patients.

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“…Additionally, activation of the Wnt signaling pathway reportedly controls the stemness of CSCs in different types of cancers including hepatocellular carcinoma (HCC), and colon, lung, and other cancers. [144][145][146][147][148] According to clinical practice, targeted treatment using MEKi (selumetinib, trametinib, and PD318088) inadvertently increased Wnt activity and led to enhanced stemness and tumor relapse in colorectal cancer. 149 Similarly, valproic acid, which was originally regarded as a histone deacetylase (HDAC) inhibitor in breast cancer treatment, can activate Wnt signaling pathway and promote the pool of mammary CSCs, leading to tumor progression.…”

Section: Epigenetic Mechanismsmentioning

confidence: 99%

Tumor cell plasticity in targeted therapy-induced resistance: mechanisms and new strategies

Pang

Yang

et al. 2023

Sig Transduct Target Ther

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Despite the success of targeted therapies in cancer treatment, therapy-induced resistance remains a major obstacle to a complete cure. Tumor cells evade treatments and relapse via phenotypic switching driven by intrinsic or induced cell plasticity. Several reversible mechanisms have been proposed to circumvent tumor cell plasticity, including epigenetic modifications, regulation of transcription factors, activation or suppression of key signaling pathways, as well as modification of the tumor environment. Epithelial-to-mesenchymal transition, tumor cell and cancer stem cell formation also serve as roads towards tumor cell plasticity. Corresponding treatment strategies have recently been developed that either target plasticity-related mechanisms or employ combination treatments. In this review, we delineate the formation of tumor cell plasticity and its manipulation of tumor evasion from targeted therapy. We discuss the non-genetic mechanisms of targeted drug-induced tumor cell plasticity in various types of tumors and provide insights into the contribution of tumor cell plasticity to acquired drug resistance. New therapeutic strategies such as inhibition or reversal of tumor cell plasticity are also presented. We also discuss the multitude of clinical trials that are ongoing worldwide with the intention of improving clinical outcomes. These advances provide a direction for developing novel therapeutic strategies and combination therapy regimens that target tumor cell plasticity.

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Cellular retinol binding protein-1 inhibits cancer stemness via upregulating WIF1 to suppress Wnt/β-catenin pathway in hepatocellular carcinoma

Cited by 17 publications

References 57 publications

RBP1 promotes the progression of eyelid basal cell carcinoma via regulating OGN expression

RBP1 promotes the progression of eyelid basal cell carcinoma via regulating OGN expression

Construction of a Necroptosis-Related miRNA Signature for Predicting the Prognosis of Patients With Hepatocellular Carcinoma

Tumor cell plasticity in targeted therapy-induced resistance: mechanisms and new strategies

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