Notch1 signaling in melanoma cells promoted tumor-induced immunosuppression via upregulation of TGF-β1

Yang, Zike; Qi, Yanxia; Lai, Nan; Zhang, Jiahe; Chen, Zehong; Li, Mingyu; Zhang, Wan; Luo, Rong; Kang, Shijun

doi:10.1186/s13046-017-0664-4

Cited by 320 publications

(197 citation statements)

References 28 publications

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“…NOTCH1 is involved in the regulation of the Akt/mTOR signaling pathway (46,47), which is widely acknowledged to promote cancer development (22)(23)(24)(25)(26)42). The present study revealed that shHSP27 decreased NOTCH1 expression, indicating that HSP27 might regulate chemoresistance in colon cancer cells via NOTCH1 and that NOTCH1 might regulate of HSP27 in the Akt/mTOR signaling pathway.…”

Section: Discussionsupporting

confidence: 49%

“…Furthermore, cross-talk among the notch receptor 1 (NOTCH1), mTOR and PI3K/Akt signaling pathways is associated with apoptosis (21). The binding of NOTCH1 to its ligands allows DNA-binding proteins to regulate the expression of NOTCH1 target genes, which are involved in the proliferation, differentiation and apoptosis of various tumor cells (22)(23)(24). Additionally, PI3K and its effectors, including Akt and mTOR, play a key role in the proliferation and survival of tumor cells (25).…”

Section: Introductionmentioning

confidence: 99%

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Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

Liu

Long

et al. 2020

Oncol Lett

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Multidrug resistance in cancer cells is a primary factor affecting therapeutic efficacy. Heat shock 27 kD protein 1 (HSP27) is associated with cell apoptosis and resistance to chemotherapy. However, the mechanisms underlying HSP27-associated pathways in colon cancer cells remain unclear. Therefore, the present study used short hairpin (sh) RNA to inhibit HSP27 expression in colon cancer cells in order to investigate the effects in vitro and in vivo. Flow cytometry was used to investigate cell apoptosis and a xenograft model was employed to examine the tumorigenesis. Protein expression was measured by Western blotting. The results revealed that suppression of HSP27 expression significantly increased cell apoptosis, inhibited tumor growth and enhanced sensitivity to the anti-cancer agents 5-fluorouracil (5-FU) and vincristine (VCR). shHSP27 significantly decreased the expression of notch receptor 1 and the phosphorylation level of Akt and mTOR, and enhanced the effect of 5-FU and VCR. In conclusion, HSP27 suppression enhanced the sensitivity of colon cancer cells to 5-FU and VCR, and increased colon cancer cell apoptosis with and without chemotherapy. Therefore, the development of novel therapeutic agents that inhibit the expression of HSP27 may offer a new treatment option for colon cancer.

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Section: Discussionsupporting

confidence: 49%

Section: Introductionmentioning

confidence: 99%

Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

Liu

Long

et al. 2020

Oncol Lett

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“…Chemokines and related cytokines in tumor microenvironment play a key role in the migration of MDSCs to tumor sites to perform immunosuppressive function. MDSCs are regulated by various cytokines and chemokines such as granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), granulocyte colony‐stimulating factor (G‐CSF), CCL2, CCL3, CXCL1, and CXCL2 . Recent studies have reported that in the animal model of endometriosis, chemokines CCL1/2/5 promote the migration of CXCR2 + MDSC to heterotopic grafts, performing immunosuppressive function .…”

Section: Main Functional Characteristics Of Mdscsmentioning

confidence: 99%

Myeloid‐derived suppressor cells: Roles in the tumor microenvironment and tumor radiotherapy

Yin

Wang

et al. 2018

Intl Journal of Cancer

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Cancer progression is closely related to the tumor microenvironment in which the tumor exists, including surrounding blood vessels, immune cells, fibroblasts, bone marrow-derived inflammatory cells, signaling molecules and the extracellular matrix. Tumors can influence the microenvironment by releasing extracellular signals, promoting tumor angiogenesis and inducing peripheral immune tolerance, while the immune cells in the microenvironment can impact the growth and evolution of cancerous cells. One of major cell components in the tumor microenvironment is myeloid-derived suppressor cells (MDSCs), which promote tumor growth and metastasis directly or indirectly by recognizing other immune cells, producing cytokines and exerting their immunosuppression functions. MDSCs have emerged as major regulators of immune responses in cancer and key targets for treating cancer. There are many limitations and side-effect in approaches of conventional cancer therapy, including radiotherapy. It has grown up to be a burgeoning field that a combination of radiotherapy and immunotherapy applied to cancer therapy. Therefore, it is fundamental to explore the immune mechanism in the process of cancer treatment. Here, we reviewed the recent progress of MDSCs in roles of the tumor microenvironment and tumor radiotherapy.

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“…11 Dysregulated Notch signalling could result in various diseases, such as leukaemia, Alagille syndrome, pulmonary arterial hypertension and ventricular septal defect. 15 Notch signalling has been reported to be activated in HCC and promotes liver tumour formation. In breast cancer, JAG1 activates Notch signalling and promotes tumour metastasis.…”

Section: Introductionmentioning

confidence: 99%

Hypomethylation‐mediated activation of cancer/testis antigen KK‐LC‐1 facilitates hepatocellular carcinoma progression through activating the Notch1/Hes1 signalling

Chen

Zuo

et al. 2019

Cell Proliferation

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Objectives: Kita-Kyushu lung cancer antigen-1 (KK-LC-1) is a cancer/testis antigen reactivated in several human malignancies. So far, the major focus of studies on KK-LC-1 has been on its potential as diagnostic biomarker and immunotherapy target.However, its biological functions and molecular mechanisms in cancer progression remain unknown. Materials and Methods: Expression of KK-LC-1 in HCC was analysed using RT-qPCR,Western blot and immunohistochemistry. The roles of KK-LC-1 on HCC progression were examined by loss-of-function and gain-of-function approaches. Pathway inhibitor DAPT was employed to confirm the regulatory effect of KK-LC-1 on the downstream Notch signalling. The interaction of KK-LC-1 with presenilin-1 was determined by co-immunoprecipitation. The association of CpG island methylation status with KK-LC-1 reactivation was evaluated by methylation-specific PCR, bisulphite sequencing PCR and 5-Aza-dC treatment. Results:We identified that HCC tissues exhibited increased levels of KK-LC-1. High KK-LC-1 level independently predicted poor survival outcome. KK-LC-1 promoted cell growth, migration, invasion and epithelial-mesenchymal transition in vitro and in vivo.KK-LC-1 modulated the Notch1/Hes1 pathway to exacerbate HCC progression through physically interacting with presenilin-1. Upregulation of KK-LC-1 in HCC was attributed to hypomethylated CpG islands.

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Notch1 signaling in melanoma cells promoted tumor-induced immunosuppression via upregulation of TGF-β1

Cited by 320 publications

References 28 publications

Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

Myeloid‐derived suppressor cells: Roles in the tumor microenvironment and tumor radiotherapy

Hypomethylation‐mediated activation of cancer/testis antigen KK‐LC‐1 facilitates hepatocellular carcinoma progression through activating the Notch1/Hes1 signalling

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