Suppression of CLEC3A inhibits osteosarcoma cell proliferation and promotes their chemosensitivity through the AKT1/mTOR/HIF1α signaling pathway

Ren, Chong; Pan, Runsang; Hou, Lianping; Wu, Huaping; Sun, Junkang; Zhang, Wenguang; Tian, Xiaobin; Chen, Houping

doi:10.3892/mmr.2020.10986

Cited by 7 publications

(9 citation statements)

References 33 publications

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“…These genes included PTPN21 (28), ST6GALNAC3 (29), FAM13A (30), and CHRNA7 (31), which were correlated with metastasis. These genes were also enriched in the PI3K/Akt, Notch1/Hes1 or Akt1/ mTOR signaling pathways and were reported to be correlated with LNM in breast cancer (32)(33)(34)(35). The NMRK2 gene was identified as an important target for mitochondrial respiration, and mitochondrial respiration is frequently dependent on metastatic cells (36,37).…”

Section: Discussionmentioning

confidence: 98%

Development and validation of a radiogenomics model to predict axillary lymph node metastasis in breast cancer integrating MRI with transcriptome data: A multicohort study

Chen

Xiao

et al. 2022

Front. Oncol.

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IntroductionTo develop and validate a radiogenomics model for predicting axillary lymph node metastasis (ALNM) in breast cancer compared to a genomics and radiomics model.MethodsThis retrospective study integrated transcriptomic data from The Cancer Genome Atlas with matched MRI data from The Cancer Imaging Archive for the same set of 111 patients with breast cancer, which were used as the training and testing groups. Fifteen patients from one hospital were enrolled as the external validation group. Radiomics features were extracted from dynamic contrast-enhanced (DCE)-MRI of breast cancer, and genomics features were derived from differentially expressed gene analysis of transcriptome data. Boruta was used for genomics and radiomics data dimension reduction and feature selection. Logistic regression was applied to develop genomics, radiomics, and radiogenomics models to predict ALNM. The performance of the three models was assessed by receiver operating characteristic curves and compared by the Delong test.ResultsThe genomics model was established by nine genomics features, and the radiomics model was established by three radiomics features. The two models showed good discrimination performance in predicting ALNM in breast cancer, with areas under the curves (AUCs) of 0.80, 0.67, and 0.52 for the genomics model and 0.72, 0.68, and 0.71 for the radiomics model in the training, testing and external validation groups, respectively. The radiogenomics model integrated with five genomics features and three radiomics features had a better performance, with AUCs of 0.84, 0.75, and 0.82 in the three groups, respectively, which was higher than the AUC of the radiomics model in the training group and the genomics model in the external validation group (both P < 0.05).ConclusionThe radiogenomics model combining radiomics features and genomics features improved the performance to predict ALNM in breast cancer.

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Section: Discussionmentioning

confidence: 98%

Development and validation of a radiogenomics model to predict axillary lymph node metastasis in breast cancer integrating MRI with transcriptome data: A multicohort study

Chen

Xiao

et al. 2022

Front. Oncol.

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“…Compelling research has revealed that PI3K/AKT/mTOR signalling could participate in promoting the osteosarcoma process by regulating a variety of target genes. 25 The AKT1/mTOR axis might be involved in the disease progression of melanoma and F I G U R E 4 Overexpression of HK2 weakens the inhibitory effect of sh-SPI1 on the proliferation, metastasis and glycolysis of melanoma cells. A375 cells were cotransfected with sh-SPI1 and oe-HK2.…”

Section: Discussionmentioning

confidence: 99%

“…Compelling research has revealed that PI3K/AKT/mTOR signalling could participate in promoting the osteosarcoma process by regulating a variety of target genes 25 . The AKT1/mTOR axis might be involved in the disease progression of melanoma and modulated by minichromosome maintenance protein 7 (MCM7) 26 .…”

Section: Discussionmentioning

confidence: 99%

SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway

Qiu

Gao

Gong

et al. 2023

J Cellular Molecular Medi

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Spi‐1 proto‐oncogene (SPI1) plays a vital role in carcinogenesis. Our work aimed to investigate the potential regulatory mechanism of SPI1 in melanoma. The mRNA and protein levels were measured via qRT–PCR and Western blotting. Cell viability was assessed by CCK‐8 assay. The target relationship between SPI1 and hexokinase 2 (HK2) was determined using dual‐luciferase reporter detection. ChIP was conducted to confirm the targeted relationship between SPI1 and the HK2 promoter. Immunohistochemistry analysis was conducted to measure the positive cell number of SPI1 and HK2 in melanoma tissues. The cell migration abilities were determined using a wound healing assay. Glucose consumption, pyruvate dehydrogenase activity, lactate production and ATP levels were measured to assess glycolysis. SPI1 transcription in melanoma cells and tissues was dramatically higher than that in adjacent normal tissues and epidermal melanocyte HEMa‐LP, respectively. Knockdown of SPI1 restrained cell viability, metastasis and glycolysis in melanoma cells. SPI1 directly targeted HK2, and knockdown of SPI1 repressed HK2 expression. Overexpression of HK2 weakened the inhibitory effects of SPI1 knockdown on the viability, metastasis and glycolysis of melanoma cells. The serine–threonine kinase 1 (AKT1)/mammalian target of rapamycin (mTOR) axis is involved in melanoma progression. SPI1 knockdown restrained melanoma cell proliferation, metastasis and glycolysis by regulating the AKT1/mTOR pathway.

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“…We could prove the suppression of AKT1 by miR-373-3p in ECa cell lines. AKT1 was an oncogene in several cancer diseases including osteosarcoma, pancreatic ductal adenocarcinoma, colorectal cancer, and breast cancer [32][33][34][35] .Recently, lncRNAs have been implicated in the miRNA/AKT1 axis modulation in www.nature.com/scientificreports/ human cancers. For instance, the LINC00324 counteract miR-615-5p and enhance the expression of AKT1 in lung adenocarcinoma 36 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA EIF3J-AS1 enhanced esophageal cancer invasion via regulating AKT1 expression through sponging miR-373-3p

Wei

Wang

Liang

et al. 2020

Sci Rep

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Esophageal cancer (ECa) remains a major cause of mortality across the globe. The expression of EIF3J-AS1 is altered in a plethora of tumors, but its role in ECa development and progression are undefined. Here, we show that EIF3J-AS1 is up-regulated in ECa and that its expression correlates with advanced TNM stage (P = 0.014), invasion depth (P = 0.001), positive lymph node metastasis (P < 0.001) and poor survival (OS: P = 0.0059; DFS: P = 0.0037) in ECa. Functional experiments showed that knockdown EIF3J-AS1 inhibited ECa growth and metastasis through in vitro and in vivo experiments. Regarding the mechanism, EIF3J-AS1/miR-373-3p/AKT1 established the ceRNA network involved in the modulation of cell progression of ECa cells. Overall, EIF3J-AS1 may exhibit an oncogenic function in ECa via acting as a sponge for miR-373-3p to up-regulate AKT1 mRNA level, and may serve as a potential therapeutic target and a prognostic biomarker for ECa patients. Esophageal cancer (ECa) is of particularly high incidence in Chinese males compared to other regions and remains a global threat to human health. Up to ~ 450,000 new cases of ECa are diagnosed annually, of which up to ~ 400,000 of those afflicted do not survive 1. Diagnostic and therapeutic advances have been made to improve ECa therapeutics, including biopsies, chromo endoscopy and narrow-band imaging 2. However, despite these improvements, the efficiency of ECa therapies and subsequent patient prognosis remains poor. ECa therefore remains a global health burden for which new diagnostics and effective therapeutic strategies are urgently required 3. A further understanding of the molecular regulators of ECa tumorigenesis is required to expedite the discovery of novel anti-ECa strategies. While lncRNAs (long noncoding RNAs; more than 200 bases long 4-8 are not capable of translating proteins, their dysregulation is observed several cancers, such as ECa 9-12. For instance, the process of EMT (epithelialmesenchymal transition) is enhanced by lncRNA PVT1 via E-cadherin suppression in ECa 13. Further, significantly enhanced level of CASC11 was observed in ECa tissues while its silencing impeded the progression of ECa by regulating KLF6 expression 14. Previous study reported that up-regulated a novelty EIF3J-AS1 was associated with poor survival and accelerated HCC progression via targeting miR-122e5p/CTNND2 axis under hypoxia 15. Meanwhile, EIF3J-AS1 induced by H3K27 promoted colorectal cancer proliferation and inhibited apoptosis via miR-3163/YAP1 axis 16. Nevertheless, the role and inherent mechanisms of EIF3J-AS1 in human ECa development remains to be assessed. In this research, we examined the increased expression of EIF3J-AS1 in ECa cell lines and tissues, the effect of EIF3J-AS1 knocked down on inhibiting the metastasis and growth of ECa cell lines in vitro and vivo. We also examined the role of EIF3J-AS1 in ECa cells' aggressive phenotypes by miR-373-3p binding and assessing the AKT1 expression. Materials and methods Tissue specimens. Collection of a total of 182 ECa cases...

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Suppression of CLEC3A inhibits osteosarcoma cell proliferation and promotes their chemosensitivity through the AKT1/mTOR/HIF1α signaling pathway

Cited by 7 publications

References 33 publications

Development and validation of a radiogenomics model to predict axillary lymph node metastasis in breast cancer integrating MRI with transcriptome data: A multicohort study

Development and validation of a radiogenomics model to predict axillary lymph node metastasis in breast cancer integrating MRI with transcriptome data: A multicohort study

SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway

LncRNA EIF3J-AS1 enhanced esophageal cancer invasion via regulating AKT1 expression through sponging miR-373-3p

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