&lt;p&gt;Hypoxic non-small-cell lung cancer cell-derived exosomal miR-21 promotes resistance of normoxic cell to cisplatin&lt;/p&gt;

Dong, Congcong; Liu, Xingwang; Wang, Huisheng; Li, Jutao; Dai, Lei; Li, Jun

doi:10.2147/ott.s186922

Cited by 41 publications

(33 citation statements)

References 43 publications

(62 reference statements)

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“…Furthermore, aberrant miRNA expression has been demonstrated in lung cancer, which contributes to carcinogenesis and cancer development by either promoting oncogene expression or inhibiting tumor suppressor genes (27). miR-140-5p was found to serve a role in carcinogenesis of NSCLC (21,22). Target genes associated with miR-140-5p may serve as biomarkers and aid in the diagnosis and prognostic prediction of NSCLC (28,29).…”

Section: Discussionmentioning

confidence: 99%

“…Target genes associated with miR-140-5p may serve as biomarkers and aid in the diagnosis and prognostic prediction of NSCLC (28,29). The miR-140-5p/monocyte to macrophage differentiation-associated (MMD) axis could affect cell proliferation and invasion of lung cancer cells by regulating the Erk signaling pathway (21,22). In the present study, miR-140-5p expression was demonstrated to be markedly decreased in NSCLC tissues compared with normal adjacent tissues.…”

Section: Discussionmentioning

confidence: 99%

“…However, whether miR-140-5p may inhibit proliferation and induce apoptosis of NSCLC cells via targeting of YES1 remains unclear. Differential expression of miR-140-5p has been revealed in numerous signaling pathways associated with the regulation of cell apoptosis (21,22). A previous study demonstrated that the YES1 is a target gene of miR-140-5p (35).…”

Section: Discussionmentioning

confidence: 99%

“…miRNAs associated with different types of cancer include oncogenic miRNAs, tumor suppressive miRNAs and miRNA regulators (16). Previous studies have indicated that miRNA-140-5p serves an important role in numerous tumor types (17)(18)(19)(20); however, studies investigated the association between miR-140-5p expression and clinical outcomes in patients with resected NSCLC are limited and have demonstrated contradictory results (21,22). Therefore, the specific role of miR-140-5p in NSCLC remains to be determined.…”

Section: Effect Of Mir-140-5p On the Regulation Of Proliferation And mentioning

confidence: 99%

“…Micro (mi)RNAs (miRs) are a class of small (19)(20)(21)(22)(23)(24) nucleotides in length), highly conserved non-coding RNAs that may bind to the 3'-untranslated regions (3'-UTRs) of target mRNAs and subsequently suppress the translation of such RNAs to proteins (6). It has become increasingly evident that different miRNAs may either exhibit oncogenic or tumor-suppressive roles in numerous pathways, depending on their target genes or cellular context (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

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Effect of miR‑140‑5p on the regulation of proliferation and apoptosis in NSCLC and its underlying mechanism

et al. 2019

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Non-small cell lung cancer (NSCLC) is the most common type of lung cancer accounting for ~80% of lung cancer cases. According to novel research, numerous microRNAs (miRs) have been suggested to function as important regulators of cancer. In addition, the expression of miR-140-5p is decreased in patients with NSCLC. Therefore, it is important to further elucidate the role of miR-140-5p in NSCLC. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used in order to investigate the expression of miR-140-5p in NSCLC tissues and matched normal tissues and to determine miR-140-5p levels following transfection with mimics into A549 lung cancer cells. Targetscan software was used to predict the oncogene target of miR-140-5p. This analysis revealed that YES proto-oncogene 1 (YES1) includes a target site for miR-140-5p binding. The results revealed that YES1 is a potential target gene of miR-140-5p, and this was further confirmed by the results of luciferase reporter assays, which demonstrated that miR-140-5p directly targeted the predicted binding site in the 3'-untranslated region of YES1. Cell Counting Kit-8 (CCK-8) and flow cytometry assays were performed to determine the levels of cell viability and apoptosis. Western blot assays was performed to investigate the expression levels of YES1 and proteins associated with apoptosis in A549 cells following transfection. The results revealed that miR-140-5p expression was significantly downregulated in NSCLC tissues compared with matched normal tissues. The expression of miR-140-5p was significantly increased following transfection with miR-140-5p mimics. The results of CCK-8 and flow cytometry assays indicated that miR-140-5p inhibited proliferation and induced apoptosis of tumor cells. Western blot analysis and RT-qPCR revealed that YES1 and B-cell lymphoma 2 (Bcl-2) mRNA and protein expression levels were markedly decreased in A549 cells, while Bcl-2 associated X (Bax) and caspase-3 expression levels increased significantly following transfection with miR-140-5p mimics compared with the negative control group. In conclusion, miR-140-5p may induce apoptosis in A549 cells by targeting YES1 and regulating the expression of apoptosis-associated proteins Bcl-2, Bax and caspase-3.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Effect Of Mir-140-5p On the Regulation Of Proliferation And mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of miR‑140‑5p on the regulation of proliferation and apoptosis in NSCLC and its underlying mechanism

et al. 2019

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Extracellular Vesicles in Cancer Drug Resistance: Roles, Mechanisms, and Implications

Yang

et al. 2022

Advanced Science

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Extracellular vesicles (EVs) are cell-derived nanosized vesicles that mediate cell-to-cell communication via transporting bioactive molecules and thus are critically involved in various physiological and pathological conditions. EVs contribute to different aspects of cancer progression, such as cancer growth, angiogenesis, metastasis, immune evasion, and drug resistance. EVs induce the resistance of cancer cells to chemotherapy, radiotherapy, targeted therapy, antiangiogenesis therapy, and immunotherapy by transferring specific cargos that affect drug efflux and regulate signaling pathways associated with epithelial-mesenchymal transition, autophagy, metabolism, and cancer stemness. In addition, EVs modulate the reciprocal interaction between cancer cells and noncancer cells in the tumor microenvironment (TME) to develop therapy resistance. EVs are detectable in many biofluids of cancer patients, and thus are regarded as novel biomarkers for monitoring therapy response and predicting prognosis. Moreover, EVs are suggested as promising targets and engineered as nanovehicles to deliver drugs for overcoming drug resistance in cancer therapy. In this review, the biological roles of EVs and their mechanisms of action in cancer drug resistance are summarized. The preclinical studies on using EVs in monitoring and overcoming cancer drug resistance are also discussed.

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Cisplatin‐resistant osteosarcoma cell‐derived exosomes confer cisplatin resistance to recipient cells in an exosomal circ_103801‐dependent manner

Pan

Lin

2020

Cell Biology International

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Studies have shown that exosomes can mediate the chemoresistance of drug‐resistant cells by transmitting circular RNAs (circRNAs). However, the role of exosome‐derived hsa_circ_103801 (exosomal hsa_circ_103801) in osteosarcoma (OS) remains unclear. The level of hsa_circ_103801 was upregulated in the serum exosomes from patients with OS, and OS patients with high hsa_circRNA_103801 expression had a shorter survival time relative to patients with low hsa_circ_103801 expression. The expression of hsa_circ_103801 was upregulated in cisplatin‐resistant MG63 (MG63/CDDP) cells compared with that in MG63 cells. In addition, hsa_circ_103801 was highly enriched in exosomes derived from CDDP‐resistant OS cells and could be delivered to MG63 and U2OS cells through exosomes. Exosomes derived from CDDP‐resistant cells were shown to reduce the sensitivity of MG63 and U2OS cells to CDDP, inhibit apoptosis, and increase the expression of multidrug resistance‐associated protein 1 and P‐glycoprotein. Moreover, exosomal hsa_circ_103801 could strengthen the promotive effect of exosomes on the chemoresistance of MG63 and U2OS cells to CDDP. Hence, serum exosomal hsa_circ_103801 may serve as an effective prognostic biomarker for OS, and exosomal hsa_circ_103801 could be a potential target for overcoming OS chemoresistance.

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<p>Hypoxic non-small-cell lung cancer cell-derived exosomal miR-21 promotes resistance of normoxic cell to cisplatin</p>

Cited by 41 publications

References 43 publications

Effect of miR‑140‑5p on the regulation of proliferation and apoptosis in NSCLC and its underlying mechanism

Effect of miR‑140‑5p on the regulation of proliferation and apoptosis in NSCLC and its underlying mechanism

Extracellular Vesicles in Cancer Drug Resistance: Roles, Mechanisms, and Implications

Cisplatin‐resistant osteosarcoma cell‐derived exosomes confer cisplatin resistance to recipient cells in an exosomal circ_103801‐dependent manner

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