Silencing NOB1 Can Affect Cell Proliferation and Apoptosis Via the C-Jun N-Terminal Kinase Pathway in Colorectal Cancer

Zhong, Ren; Yao, Ling; Liu, Jingzheng; Qi, Zhipeng; Li, Jian

doi:10.1080/08941939.2019.1697401

Cited by 3 publications

(4 citation statements)

References 35 publications

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“…Its mutation in the promoter region is associated with increased CRC risk by elevating promoter activity [49]. JUN plays a key role in regulating and promoting the signaling pathways related to carcinogenesis, cell proliferation, metabolism, migration, apoptosis, and survival [50][51][52]. EGFR, the ErbB family of related cell membrane receptors, is a receptor tyrosine kinase binding ligand of the EGF family.…”

Section: Discussionmentioning

confidence: 99%

A network pharmacology-based investigation on the bioactive ingredients and molecular mechanisms of Gelsemium elegans Benth against colorectal cancer

Que

Chen

Yang

et al. 2021

BMC Complement Med Ther

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Background Colorectal cancer (CRC) remains one of the leading causes of cancer-related death worldwide. Gelsemium elegans Benth (GEB) is a traditional Chinese medicine commonly used for treatment for gastrointestinal cancer, including CRC. However, the underlying active ingredients and mechanism remain unknown. This study aims to explore the active components and the functional mechanisms of GEB in treating CRC by network pharmacology-based approaches. Methods Candidate compounds of GEB were collected from the Traditional Chinese Medicine@Taiwan, Traditional Chinese Medicines Integrated Database, Bioinformatics Analysis Tool for Molecular mechanism of Traditional Chinese Medicine, and published literature. Potentially active targets of compounds in GEB were retrieved from SwissTargetPrediction databases. Keywords “colorectal cancer”, “rectal cancer” and “colon cancer” were used as keywords to search for related targets of CRC from the GeneCards database, then the overlapped targets of compounds and CRC were further intersected with CRC related genes from the TCGA database. The Cytoscape was applied to construct a graph of visualized compound-target and pathway networks. Protein-protein interaction networks were constructed by using STRING database. The DAVID tool was applied to carry out Gene Ontology and Kyoto Encyclopedia of Genes and Genome pathway enrichment analysis of final targets. Molecular docking was employed to validate the interaction between compounds and targets. AutoDockTools was used to construct docking grid box for each target. Docking and molecular dynamics simulation were performed by Autodock Vina and Gromacs software, respectively. Results Fifty-three bioactive compounds were successfully identified, corresponding to 136 targets that were screened out for the treatment of CRC. Functional enrichment analysis suggested that GEB exerted its pharmacological effects against CRC via modulating multiple pathways, such as pathways in cancer, cell cycle, and colorectal cancer. Molecular docking analysis showed that the representative compounds had good affinity with the key targets. Molecular dynamics simulation indicated that the best hit molecules formed a stable protein-ligand complex. Conclusion This network pharmacology study revealed the multiple ingredients, targets, and pathways synergistically involved in the anti-CRC effect of GEB, which will enhance our understanding of the potential molecular mechanism of GEB in treatment for CRC and lay a foundation for further experimental research.

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Section: Discussionmentioning

confidence: 99%

A network pharmacology-based investigation on the bioactive ingredients and molecular mechanisms of Gelsemium elegans Benth against colorectal cancer

Que

Chen

Yang

et al. 2021

BMC Complement Med Ther

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“…Here, using dual‐luciferase assays, we found that Lnc00113 could bind directly to miR‐107. NOB1, identified as an oncogene, exhibits upregulation during the development of several cancers, including papillary thyroid cancer, prostate cancer and breast cancer 31,32 . Moreover, NOB1 is regulated by a variety of miRNAs in several cancer types.…”

Section: Discussionmentioning

confidence: 99%

“…NOB1, identified as an oncogene, exhibits upregulation during the development of several cancers, including papillary thyroid cancer, prostate cancer and breast cancer. 31,32 Moreover, NOB1 is regulated by a variety of miRNAs in several cancer types. For instance, miR-363 inhibits cell proliferation and induces apoptosis by directly targeting NOB1.…”

Section: Discussionmentioning

confidence: 99%

Lnc00113 promotes triple‐negative breast cancer progression via the NOB‐1/MAPK signaling axis

Li,

Jin,

Huang

et al. 2024

The Journal of Gene Medicine

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BackgroundTriple‐negative breast cancer (TNBC) represents the most aggressive form of breast cancer. While the involvement of long non‐coding RNA (lncRNA) in the progression of TNBC has been demonstrated, the role of Lnc00113 in TNBC remains unexplored. We aimed to explore the function of Lnc00113 in TNBC.MethodsExpression levels and the clinical significance of Lnc00113 were assessed in The Cancer Genome Atlas (TCGA) database. The expression levels of Lnc00113 in TNBC tissues and cell lines were examined using qRT‐PCR (quantitative Real‐Time Polymerase chain reaction). The proliferation, apoptosis and invasion abilities were evaluated using CCK‐8 (Cell Counting Kit‐8), EdU (5‐Ethynyl‐2'‐deoxyuridine), apoptosis and transwell assays following Lnc00113 knockdown/overexpression. Dual‐luciferase and fluorescence in situ hybridization assays were employed to detect the correlation between Lnc00113, miR‐107 and Nin‐one binding protein (NOB‐1).ResultsWe identified significant upregulation of Lnc00113 in TNBC tissues and cell lines, with high Lnc00113 expression correlating with advanced pathological staging and poorer prognosis in the TCGA database. Functional assessments through knockdown/overexpression experiments revealed that Lnc00113 promoted TNBC cell proliferation, apoptosis and invasion. Fluorescence in situ hybridization experiments showed cytoplasmic localization of both Lnc00113 and NOB‐1. Dual‐luciferase assays demonstrated direct binding between Lnc00113 and miR‐107, while miR‐107 directly interacted with NOB‐1. Mechanistically, our findings indicated that Lnc00113 promotes TNBC progression through the miR‐107/NOB‐1/MAPK signaling axis.ConclusionLnc00113 emerges as a potential driver of TNBC growth and progression through modulation of the NOB‐1/MAPK signaling axis, providing insights into diagnostic biomarkers and therapeutic targets for TNBC.

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“…NOB1 plays an important role in the biosynthesis of ribosome small subunit and 26S proteasome. NOB1 may be an oncogene, which promotes the proliferation of cervical cancer, papillary thyroid cancer and other malignant tumors [15][16][17]. miR-363 regulate the cell proliferation, migration and EMT through target the expression of NOB1 [18].…”

Section: Discussionmentioning

confidence: 99%

Sublethal heat treatment promotes breast cancer metastasis and its molecular mechanism revealed by quantitative proteomic analysis

Xia

et al. 2022

Aging

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Radiofrequency ablation (RFA) is a frequently used thermal ablation technique for breast tumors. The study aimed to identify the effect of sublethal heat treatment on biological function of breast cancer cells and reveal its potential molecular mechanism. The expression profile of dysregulated proteins in sublethal heat treated breast cancer cells was analyzed by quantitative proteomic analysis. The differentially expressed proteins in the sublethal heat treated breast cancer were identified. The potential biological functions of these proteins were evaluated. The proliferation and invasion ability of breast cancer cells were enhanced after sublethal heat treatment. The expression profile of proteins in sublethal heat treated breast cancer cells was abundant, and most of which were newly discovered. A total of 206 differentially expressed proteins were identified. Among them, 101 proteins were downregulated while 105 proteins were upregulated. GO and KEGG analysis indicated that various systems were involved in the process of sublethal heat treatment including cancer, immune system, et al. Immunohistochemistry staining showed that the expression of Heat shock protein 1B, NOB1 and CRIP1 was highly expressed while the expression of BCLAF1 was lower in sublethal heat treated group. The proliferation and invasion ability of breast cancer cells were enhanced after sublethal heat treatment. Sublethal heat treatment caused gene alterations in cancer and immune system. Heat shock protein 1B, NOB1 and CRIP1 were upregulated while BCLAF1 was downregulated in breast cancer after sublethal heat treatment.

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Silencing NOB1 Can Affect Cell Proliferation and Apoptosis Via the C-Jun N-Terminal Kinase Pathway in Colorectal Cancer

Cited by 3 publications

References 35 publications

A network pharmacology-based investigation on the bioactive ingredients and molecular mechanisms of Gelsemium elegans Benth against colorectal cancer

A network pharmacology-based investigation on the bioactive ingredients and molecular mechanisms of Gelsemium elegans Benth against colorectal cancer

Lnc00113 promotes triple‐negative breast cancer progression via the NOB‐1/MAPK signaling axis

Sublethal heat treatment promotes breast cancer metastasis and its molecular mechanism revealed by quantitative proteomic analysis

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