Homing Choices of Breast Cancer Cells Revealed by Tissue Specific Invasion and Extravasation Lab-on-a-chip Platforms

Firatligil-Yildirir, Burcu; Bati-Ayaz, Gizem; Tahmaz, Ismail; Bilgen, Muge; Pesen-Okvur, Devrim; Yalcin-Ozuysal, Özden

doi:10.1101/2020.09.25.312793

Cited by 3 publications

(3 citation statements)

References 32 publications

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“…S4B) in metastatic MDA-MB-231 relative to in parental MDA-MB-231 cells. Metastatic MDA-MB-231 (MDA-MB-231 LM2) cells constitute MDA-MB-231 cells that have metastasized to the lungs and are organ-speci c metastatic clones with strong migration and invasive properties [37]. These results support our hypothesis that miR-5088-5p expression is upregulated via suppression of its promoter methylation, which, in turn, promotes tumor malignancy.…”

Section: Ir Upregulates Biogenesis Of Mir-5088-5p Through Inhibiting ...supporting

confidence: 63%

miR-5088-5p inhibitor reduces radiation-induced malignancy by decreasing Slug

Seok

Choi

et al. 2022

Preprint

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Purpose Radiotherapy is widely used for cancer treatment, but paradoxically, surviving cancer cells can become malignant, leading to tumor recurrence or metastasis. Therefore, in order to increase the effectiveness of radiotherapy, efforts to reduce radiation-induced malignancy are absolutely necessary. As a tool, microRNA simultaneously regulates the expression of multiple target mRNAs, so it has significant potential as an effective therapeutic agent. The main objective of this study is to elucidate the malignant mechanism of radiation-induced miR-5088-5p and to prove the efficacy of miR-5088-5p inhibitor for mitigating malignancy, thereby demonstrating its applicability as a therapeutic agent to increase the efficiency of radiotherapy. Methods To analyze the relationship between radiation and miR-5088-5p expression, miR-5088-5p levels were determined by qRT-PCR in the plasma of breast and lung cancer patients with or without radiotherapy. MSP and qMSP assays were used to confirm the methylation of radiation-induced miR-5088-5p. To determine whether miR-5088-5p inhibitor reduces radiation-induced malignancy by decreasing Slug, we used wound healing, invasion, sphere formation, Western blot, qRT-PCR assays, and in vivo mouse xenograft metastatic model. Results It was confirmed at both the cellular and animal model that miR-5088-5p, which showed higher expression in the plasma of breast cancer and lung cancer patients with radiotherapy, enhances tumor malignancy by enhancing its expression through hypomethylation of its promoter by radiation. On the other hand, it was shown that miR-5088-5p inhibitor reduced the mechanism of radiation-induced malignancy. Conclusions Collectively, miR-5088-5p inhibitors have shown potential as a combination therapy to enhance radiotherapy effectiveness by reducing radiation-induced malignancy.

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Section: Ir Upregulates Biogenesis Of Mir-5088-5p Through Inhibiting ...supporting

confidence: 63%

miR-5088-5p inhibitor reduces radiation-induced malignancy by decreasing Slug

Seok

Choi

et al. 2022

Preprint

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“…CSCs contribute to anticancer therapeutic resistance, and patient survival depends on our ability to target CSCs in the treatments. [ 37–40 ] The level of spatial and temporal control provided by microfluidics incorporating 3D cell culture has opened up new avenues for research on cancer invasion, extravasation, [ 41 ] and drug response. [ 42 ] Not only have tumors‐on‐chips reduced drug development time and cost, but they have also eliminated ethical issues related to animal studies [ 43 ] and are compatible with CSC research.…”

Section: Introductionmentioning

confidence: 99%

Cancer Stem Cells in Tumor Modeling: Challenges and Future Directions

Dogan

Kısım

Bati-Ayaz

et al. 2021

Advanced NanoBiomed Research

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Microfluidic tumors‐on‐chips models have revolutionized anticancer therapeutic research by creating an ideal microenvironment for cancer cells. The tumor microenvironment (TME) includes various cell types and cancer stem cells (CSCs), which are postulated to regulate the growth, invasion, and migratory behavior of tumor cells. In this review, the biological niches of the TME and cancer cell behavior focusing on the behavior of CSCs are summarized. Conventional cancer models such as 3D cultures and organoid models are reviewed. Opportunities for the incorporation of CSCs with tumors‐on‐chips are then discussed for creating tumor invasion models. Such models will represent a paradigm shift in the cancer community by allowing oncologists and clinicians to predict better which cancer patients will benefit from chemotherapy treatments.

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“…CSCs contribute to anticancer therapeutic resistance, and patient survival depends on our ability to target CSCs in the treatments. [37][38][39][40] The level of spatial and temporal control provided by microfluidics incorporating 3D cell culture has opened up new avenues for research on cancer invasion, extravasation, [41] and drug response. [42] Not only have tumors-on-chips reduced drug development time and cost, but they have also eliminated ethical issues related to animal studies [43] and are compatible with CSC research.…”

Section: Introductionmentioning

confidence: 99%