RÉSUMÉ
BACKGROUND: Highly supported microRNAs (miRNAs) are key players in cancer development. Each of these miRNAs may act as an oncomir, a tumor-suppressor, or both in various cancers. Mir-151a-5p is believed to be one of these miRNAs with diverse roles. We have conducted this systematic review to clarify the role of mir-151a-5p in formation of various cancers. METHODS AND MATERIALS: We searched for existing articles in PubMed, Web of Science, Cochrane, Scopus, and RNAcentral databases up to November 2022. A total of 23 articles were qualified and included in the present systematic review. This review is registered on JBI at https://jbi.global/systematic-review-register. Expression levels, diagnostic and prognostic values, biological processes, and targeted downstream genes are included. RESULTS: Assembled data indicate the expression levels of mir-151a-5p vary from down- to up-regulated based on the type of the cancer. Its functional role depends on the genetic profile of cancerous tissue. Results mostly point to the oncogenic role of this miRNA in Pituitary adenomas, Acute Myeloid Leukemia (AML), Endometrial, Lung, Barrett's carcinogenesis, Colorectal, Myelodysplastic syndromes, Hepatocellular carcinoma and Breast cancers, as its inhibited targets seem to be controlling several signaling pathways, cell adhesion, and cell cycle. At the same time, tumor-suppressing role has also been observed only in Malignant Pleural Mesothelioma, Central Nerve System (CNS) lymphoma, Chronic Myeloid and Acute Lymphocytic Leukemia. Two types of cancers, prostate and colon, show contradictory results as there are studies supporting both up- and down-regulation in these cancers. Pituitary adenomas, Barrett's carcinogenesis and CNS lymphomas are top cancers diagnosed with mir-151-5p. However, prognostic feature is only applicable to Lung adenocarcinoma. DISCUSSION: Based on the present findings and further studies in the future, mir-151a-5p may be used as diagnostic and prognostic biomarkers or even a therapeutic target in cancer studies. DATA AVAILABILITY STATEMENT: The articles used in this study can be found with the defined search phrase in mentioned databases. A list of selected articles will be available on reasonable requests.
Sujet(s)
microARN , Tumeurs de l'hypophyse , Mâle , Humains , Tumeurs de l'hypophyse/génétique , microARN/génétique , microARN/métabolisme , Carcinogenèse/génétique , Transformation cellulaire néoplasique/génétique , Gènes suppresseurs de tumeur , Régulation de l'expression des gènes tumoraux/génétiqueRÉSUMÉ
BACKGROUND: Although investigating the probable side effects of post intraoperative radiotherapy wound fluid secretion (PIWFS) is crucial, especially in clinical cases, no report has been published on the effect of PIWFS on the remaining tumor cells (in the vital state) in cavity side margins or surrounding regions. These tumor cells might be directly/indirectly exposed to intraoperative radiation therapy (IORT). Here, for the first time, we investigated the effect of PIWFS on tumor cells of the same patient extracted from the excised tumor in the spheroid form. METHODS: We generated 8 human-derived breast tumor spheroids from 4 patient specimens who received to IORT, dissociated and cultured them in microfluidic devices. The spheroids from each sample were treated with the patients' PIWFS and DMEM medium separately. Two different parameters, called area and number of detached cells (NDCs), were determined and investigated to evaluate the spheroids' vital and proliferative states. RESULTS: The results showed severe transformation in tumor spheroids' function into more invasive and proliferative functions after treatment with PIWFS. CONCLUSION: Although the radiation-induced bystander effect may have a role in this observation, further experiments must be done to better clarify the probable desired or non-desired effects of post-IORT secretion for both the remaining tumor cells and the surrounding immune cells.
Sujet(s)
Tumeurs du sein , Tumeurs du sein/anatomopathologie , Femelle , HumainsRÉSUMÉ
Doxorubicin (DOX) is an effective chemotherapy agent against a wide variety of tumors. However, intrinsic or acquired resistance diminishes the sensitivity of cancer cells to DOX, which leads to a cancer relapse and treatment failure. Resolutions to this challenge includes identification of the molecular pathways underlying DOX sensitivity/resistance and the development of innovative techniques to boost DOX sensitivity. DOX is classified as a Topoisomerase II poison, which is cytotoxic to rapidly dividing tumor cells. Molecular mechanisms responsible for DOX resistance include effective DNA repair and resumption of cell proliferation, deregulated development of cancer stem cell and epithelial to mesenchymal transition, and modulation of programmed cell death. MicroRNAs (miRNAs) have been shown to potentiate the reversal of DOX resistance as they have gene-specific regulatory functions in DOX-responsive molecular pathways. Identifying the dysregulation patterns of miRNAs for specific tumors following treatment with DOX facilitates the development of novel combination therapies, such as nanoparticles harboring miRNA or miRNA inhibitors to eventually prevent DOX-induced chemoresistance. In this article, we summarize recent findings on the role of miRNAs underlying DOX sensitivity/resistance molecular pathways. Also, we provide latest strategies for utilizing deregulated miRNA patterns as biomarkers or miRNAs as tools to overcome chemoresistance and enhance patient's response to DOX treatment.
Sujet(s)
Doxorubicine/pharmacologie , Résistance aux médicaments antinéoplasiques/effets des médicaments et des substances chimiques , Résistance aux médicaments antinéoplasiques/génétique , microARN/génétique , Tumeurs/traitement médicamenteux , Antibiotiques antinéoplasiques/pharmacologie , Apoptose/effets des médicaments et des substances chimiques , Apoptose/génétique , Prolifération cellulaire/effets des médicaments et des substances chimiques , Prolifération cellulaire/génétique , Réparation de l'ADN/effets des médicaments et des substances chimiques , Réparation de l'ADN/génétique , Régulation de l'expression des gènes tumoraux/effets des médicaments et des substances chimiques , Humains , Tumeurs/génétique , Tumeurs/thérapieRÉSUMÉ
BACKGROUND: The standard treatment for breast cancer is breast-conserving surgery (BCS) with radiotherapy. If external beam radiation therapy (EBRT) can be safely replaced with intraoperative radiotherapy (IORT), it will help patients to save their breast and to have equivocal or better results in DFS and overall survival (OS). METHODS: A total of 2022 patients with breast cancer treated during 6 years were enrolled in the current study. A total of 657, 376, and 989 patients received EBRT, radical, and boost dose by IORT, respectively, according to the IRIORT consensus protocol. The primary endpoint was recurrence and death. The secondary endpoint was the role of variables in recurrence and death. RESULTS: With a mean follow-up of 34.5 and 40.18 months for the IORT and EBRT groups, respectively, there was a significant difference in DFS between electron boost and X-ray boost groups (P=0.037) and the electron radical group compared with EBRT (P=0.025), but there was no significant difference between other boost and radical groups in DFS and OS. CONCLUSIONS: IORT can be a preferred treatment modality because of its noninferior outcomes, and in some special conditions, it has superior outcomes compared to EBRT, particularly in delivering radical dose with IORT.