Emerging agents that target signaling pathways in cancer stem cells

Yang, Yue; Li, Xiaoman; Wang, Ting; Guo, Qianqian; Xi, Tao; Zheng, Lufeng

doi:10.1186/s13045-020-00901-6

Cited by 124 publications

(119 citation statements)

References 168 publications

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“…CSCs display many characteristics of embryonic or tissue stem cells and often show continuous activation of highly conserved signaling pathways related to development and tissue homeostasis [126,127]. The Wnt/βcatenin signaling pathway is associated with regulating the pluripotency, self-renewal of stem cells and differentiation ability [1,128].…”

Section: Cancer Stem Cells -Wnt/β-catenin Signaling Pathway Inhibitorsmentioning

confidence: 99%

Targeting the Wnt/β-catenin signaling pathway in cancer

2020

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The aberrant Wnt/β-catenin signaling pathway facilitates cancer stem cell renewal, cell proliferation and differentiation, thus exerting crucial roles in tumorigenesis and therapy response. Accumulated investigations highlight the therapeutic potential of agents targeting Wnt/β-catenin signaling in cancer. Wnt ligand/ receptor interface, β-catenin destruction complex and TCF/β-catenin transcription complex are key components of the cascade and have been targeted with interventions in preclinical and clinical evaluations. This scoping review aims at outlining the latest progress on the current approaches and perspectives of Wnt/β-catenin signaling pathway targeted therapy in various cancer types. Better understanding of the updates on the inhibitors, antagonists and activators of Wnt/β-catenin pathway rationalizes innovative strategies for personalized cancer treatment. Further investigations are warranted to confirm precise and secure targeted agents and achieve optimal use with clinical benefits in malignant diseases.

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Section: Cancer Stem Cells -Wnt/β-catenin Signaling Pathway Inhibitorsmentioning

confidence: 99%

Targeting the Wnt/β-catenin signaling pathway in cancer

2020

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“…Autophagy is an evolutionally highly conserved process, which is necessary for the orderly degradation and recycling of cellular components ( Yang et al, 2020 ). In normal cells, autophagy keeps low-level constitutive function.…”

Section: Introductionmentioning

confidence: 99%

The expression characteristics and prognostic roles of autophagy-related genes in gastric cancer

Wang

Jing

et al. 2021

PeerJ

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Background Autophagy is an evolutionally highly conserved process, accompanied by the dynamic changes of various molecules, which is necessary for the orderly degradation and recycling of cellular components. The aim of the study was to identify the role of autophagy-related (ATG) genes in the occurrence and development of gastric cancer (GC). Methods Data from Oncomine dataset was used for the differential expression analysis between cancer and normal tissues. The association of ATG genes expression with clinicopathologic indicators was evaluated by The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database. Moreover, using the TCGA datasets, the prognostic role of ATG genes was assessed. A nomogram was further built to assess the independent prognostic factors. Results The expression of autophagy-related genes AMBRA1, ATG4B, ATG7, ATG10, ATG12, ATG16L2, GABARAPL2, GABARAPL1, ULK4 and WIPI2 showed differences between cancer and normal tissues. After verification, ATG14 and ATG4D were significantly associated with TNM stage. ATG9A, ATG2A, and ATG4D were associated with T stage. VMP1 and ATG4A were low-expressed in patients without lymph node metastasis. No gene in autophagy pathway was associated with M stage. Further multivariate analysis suggested that ATG4D and MAP1LC3C were independent prognostic factors for GC. The C-index of nomogram was 0.676 and the 95% CI was 0.628 to 0.724. Conclusion Our study provided a comprehensive illustration of ATG genes expression characteristics in GC. Abnormal expressions of the ubiquitin-like conjugated system in ATG genes plays a key role in the occurrence of GC. ATG8/LC3 sub-system may play an important role in development and clinical outcome of GC. In the future, it is necessary to further elucidate the alterations of specific ATG8/LC3 forms in order to provide insights for the discovery, diagnosis, or targeting for GC.

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“…Activation of the Notch signaling pathway promotes tumor proliferation and metastasis. Conversely, inhibition of this pathway can eliminate CSCs and increase drug sensitivity [39] . For example, Notch signaling is a key method to regulate the survival of CSCs in triple negative breast cancer.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MONC Suppresses the Malignant Phenotype of Endometrial Cancer Stem Cells by Regulating the MiR-636/GLCE Axis

Y¹,

Huo²,

He³

et al. 2020

Preprint

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Background: Emerging evidence shows that abnormal expression of long non-coding RNA is involved in the occurrence and development of various tumors. LncRNA MONC is abnormally expressed in head and neck squamous cell carcinoma (HNSCC), lung cancer, colorectal cancer, and acute megakaryocytic leukemia, but the biological function and potential regulatory mechanism of MONC in endometrial cancer stem cells (ECSCs) and endometrial cancer cells (ECCs) have not been studied. In this study, we aimed to explore the tumor suppressive effect and mechanism of MONC in regulating ECSCs and ECCs. Methods: The expression of genes was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The expression of proteins was detected by Western blot. The interplay of LncRNA-miRNA-mRNA was verified using the luciferase assay. The growth rate of ECSC spheroids was detected by sphere formation assay. Cell proliferation was detected by CCK-8 assay. The cell invasion was detected by transwell invasion assay. Cell cycle was detected by Cell cycle analysis.Cell apoptosis was detected by the Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double-staining assay. Animal study was conducted to evaluate the effect of MONC combined with miR-636 on tumor growth in vivo. Results: Low MONC expression in endometrial carcinoma (EC), which directly inhibits the malignant biological behavior of ECSCs and ECCs by directly inhibiting miR-636. Simultaneously, miR-636 may indirectly reduce the expression of MONC. Down-regulation of miR-636 may promote GLCE expression by targeting the 3'-untranslated region (UTR) of the downstream gene GLCE, thereby inhibiting the progression of ECSCs. MONC combined with miR-636 inhibited the Notch signaling pathway and tumor epithelial-to-mesenchymal transition (EMT) process. In addition, we verified the tumor suppressive effect of MONC in nude mice, miR-636 can rescue the tumor suppressive effect of overexpressing MONC, and this effect is more obvious in ECSC. Conclusion: MONC inhibits the malignant phenotypes of ECSCs and ECCs by regulating the miR-636/GLCE axis. The MONC/miR-636/GLCE axis may provide novel treatment avenues for human EC.

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Emerging agents that target signaling pathways in cancer stem cells

Cited by 124 publications

References 168 publications

Targeting the Wnt/β-catenin signaling pathway in cancer

Targeting the Wnt/β-catenin signaling pathway in cancer

The expression characteristics and prognostic roles of autophagy-related genes in gastric cancer

LncRNA MONC Suppresses the Malignant Phenotype of Endometrial Cancer Stem Cells by Regulating the MiR-636/GLCE Axis

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