The microRNA miR-181c enhances chemosensitivity and reduces chemoresistance in breast cancer cells via down-regulating osteopontin

Han, Bing; Huang, Jian; Han, Yunfeng; Hao, Jie; Wu, Xueya; Song, Haoming; Chen, Xuesong; Shen, Qiang; Dong, Xiaoqun; Hui, Pei; Cai, Li

doi:10.1016/j.ijbiomac.2018.12.075

Cited by 37 publications

(21 citation statements)

References 57 publications

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“…Taken together, this suggests that chemotherapy activates the JNK pathway to promote OPN-mediated chemoresistance [105]. As possible mechanisms for OPN-mediated chemoresistance, decreased activation of p53 and p38 have also been suggested [158,159].…”

Section: Breast Cancermentioning

confidence: 80%

Osteopontin: A Key Regulator of Tumor Progression and Immunomodulation

Moorman

Poschel

Klement

et al. 2020

Cancers

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OPN is a multifunctional phosphoglycoprotein expressed in a wide range of cells, including osteoclasts, osteoblasts, neurons, epithelial cells, T, B, NK, NK T, myeloid, and innate lymphoid cells. OPN plays an important role in diverse biological processes and is implicated in multiple diseases such as cardiovascular, diabetes, kidney, proinflammatory, fibrosis, nephrolithiasis, wound healing, and cancer. In cancer patients, overexpressed OPN is often detected in the tumor microenvironment and elevated serum OPN level is correlated with poor prognosis. Initially identified in activated T cells and termed as early T cell activation gene, OPN links innate cells to adaptive cells in immune response to infection and cancer. Recent single cell RNA sequencing revealed that OPN is primarily expressed in tumor cells and tumor-infiltrating myeloid cells in human cancer patients. Emerging experimental data reveal a key role of OPN is tumor immune evasion through regulating macrophage polarization, recruitment, and inhibition of T cell activation in the tumor microenvironment. Therefore, in addition to its well-established direct tumor cell promotion function, OPN also acts as an immune checkpoint to negatively regulate T cell activation. The OPN protein level is highly elevated in peripheral blood of human cancer patients. OPN blockade immunotherapy with OPN neutralization monoclonal antibodies (mAbs) thus represents an attractive approach in human cancer immunotherapy.

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Section: Breast Cancermentioning

confidence: 80%

Osteopontin: A Key Regulator of Tumor Progression and Immunomodulation

Moorman

Poschel

Klement

et al. 2020

Cancers

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“…Significantly high level of miR-216a, miR-124-3p, miR-148/152, miR-192-5p, miR-181c, miR-381, and miR-489 have been documented to be linked with DOX sensitivity in BC cell lines [85,86,[136][137][138][139][140]. Among them, miR-181c modulates drug efficiency through inactivating its downstream gene OPN (osteopontin), leading to enhanced p53-dependent transactivation and apoptosis in resistant BC cells [85]. miR-381 can enhance chemosensitization via downregulating the MAPK/FYN signaling, which ultimately overcomes drug resistance in BC patients [86].…”

Section: Bcmentioning

confidence: 99%

Role of non-coding RNAs and RNA modifiers in cancer therapy resistance

et al. 2020

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As the standard treatments for cancer, chemotherapy and radiotherapy have been widely applied to clinical practice worldwide. However, the resistance to cancer therapies is a major challenge in clinics and scientific research, resulting in tumor recurrence and metastasis. The mechanisms of therapy resistance are complicated and result from multiple factors. Among them, non-coding RNAs (ncRNAs), along with their modifiers, have been investigated to play key roles in regulating tumor development and mediating therapy resistance within various cancers, such as hepatocellular carcinoma, breast cancer, lung cancer, gastric cancer, etc. In this review, we attempt to elucidate the mechanisms underlying ncRNA/modifier-modulated resistance to chemotherapy and radiotherapy, providing some therapeutic potential points for future cancer treatment.

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“…There was an inverse correlation between the miR-181c and OPN expression levels which was associated with the DOX response, metastasis, and BC patients’ overall and disease-free survival. Moreover, miR-181c inhibited the EMT of BC cells via vimentin and N-cadherin down regulations and E-cadherin up regulation [ 161 ].…”

Section: Main Textmentioning

confidence: 99%

MicroRNAs as the critical regulators of Doxorubicin resistance in breast tumor cells

2021

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Background Chemotherapy is one of the most common treatment options for breast cancer (BC) patients. However, about half of the BC patients are chemotherapeutic resistant. Doxorubicin (DOX) is considered as one of the first line drugs in the treatment of BC patients whose function is negatively affected by multi drug resistance. Due to the severe side effects of DOX, it is very important to diagnose the DOX resistant BC patients. Therefore, assessment of molecular mechanisms involved in DOX resistance can improve the clinical outcomes in BC patients by introducing the novel therapeutic and diagnostic molecular markers. MicroRNAs (miRNAs) as members of the non-coding RNAs family have pivotal roles in various cellular processes including cell proliferation and apoptosis. Therefore, aberrant miRNAs functions and expressions can be associated with tumor progression, metastasis, and drug resistance. Moreover, due to miRNAs stability in body fluids, they can be considered as non-invasive diagnostic markers for the DOX response in BC patients. Main body In the present review, we have summarized all of the miRNAs that have been reported to be associated with DOX resistance in BC for the first time in the world. Conclusions Since, DOX has severe side effects; it is required to distinguish the non DOX-responders from responders to improve the clinical outcomes of BC patients. This review highlights the miRNAs as pivotal regulators of DOX resistance in breast tumor cells. Moreover, the present review paves the way of introducing a non-invasive panel of prediction markers for DOX response among BC patients.

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The microRNA miR-181c enhances chemosensitivity and reduces chemoresistance in breast cancer cells via down-regulating osteopontin

Cited by 37 publications

References 57 publications

Osteopontin: A Key Regulator of Tumor Progression and Immunomodulation

Osteopontin: A Key Regulator of Tumor Progression and Immunomodulation

Role of non-coding RNAs and RNA modifiers in cancer therapy resistance

MicroRNAs as the critical regulators of Doxorubicin resistance in breast tumor cells

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