Article
Biochemistry & Molecular Biology
Masashi Kawami, Shinnosuke Takenaka, Mizuki Akai, Ryoko Yumoto, Mikihisa Takano
Summary: The study revealed that in p53-wild type NSCLC cells, miR-34a led to an upregulation of α-SMA, enhanced p53 activity, and promoted cell migration. However, these effects were not significant in p53-deficient cells. Under p53-knockdown condition, miR-34a only upregulated α-SMA, illustrating a close relationship between p53 and miR-34a-induced EMT in p53-wild type NSCLC cells.
Article
Biochemistry & Molecular Biology
Chunfeng Liu, Matjaz Rokavec, Zekai Huang, Heiko Hermeking
Summary: This study reveals that curcumin can activate the KEAP1/NRF2/ARE pathway and induce ROS to upregulate the expression of miR-34 in colorectal cancer cells. Curcumin can also inhibit migration and invasion of cancer cells and promote mesenchymal-epithelial transition by activating this pathway. Therefore, activation of the KEAP1/NRF2/miR-34 axis may contribute to the tumor suppressive effects of curcumin.
CELL DEATH AND DIFFERENTIATION
(2023)
Article
Biochemistry & Molecular Biology
Sophie Mockly, Elisabeth Houbron, Herve Seitz
Summary: miR-34a does not meet the definition of tumor suppressor miRNAs, as it is not down-regulated in primary tumors and does not exhibit anti-tumorigenic activity. Therefore, synthetic administration of miR-34a is not efficient against solid tumors.
NUCLEIC ACIDS RESEARCH
(2022)
Article
Oncology
Lan Ge, Yaguang Wu, Ming Wan, Yi You, Zhifang Zhai, Zhiqiang Song
Summary: The study revealed that cisplatin increased the secretion of miR-34a by exosomes in melanoma cells, contributing to drug resistance, while metformin sensitized melanoma cells to cisplatin. The findings suggest a promising therapeutic strategy of combining metformin with cisplatin for melanoma treatment.
JOURNAL OF ONCOLOGY
(2021)
Article
Chemistry, Multidisciplinary
Esra Dirimtekin, Maria Mortoglou, Ceren Alavanda, Asmaa Benomar Yemlahi, Esra Arslan Ates, Ilter Guney, Pinar Uysal-Onganer
Summary: miR-34a is downregulated and associated with inhibition of tumor growth and invasion in ovarian cancer, while FOXP1 is reported as either an oncogene or tumor suppressor. It is found that miR-34a and FOXP1 are reversely correlated, and inhibition of miR-34a leads to upregulation of FOXP1 expression and increased cellular invasion. miR-34a could be a potential biomarker for improving the diagnostic efficiency of ovarian cancer, and its overexpression may reduce pathogenesis by targeting FOXP1.
Article
Environmental Sciences
Rili Hao, Xinyu Song, Dongxiao Sun-Waterhouse, Xintong Tan, Feng Li, Dapeng Li
Summary: The study found that cadmium can induce renal damage in mice through inflammation and apoptosis via the miR-34a/Sirt1/p53 axis. This is the first report on the role of miR-34a/Sirt1/p53 axis in regulating cadmium-induced apoptosis and nephrotoxicity in mice, providing new insights into miRNA-based regulation of heavy metal induced-nephrotoxicity.
ENVIRONMENTAL POLLUTION
(2021)
Article
Cell Biology
Junhua Gong, Minghua Cong, Hao Wu, Menghao Wang, He Bai, Jingyuan Wang, Keting Que, Kaiwen Zheng, Wenfeng Zhang, Xiaoli Yang, Jianping Gong, Hanping Shi, Mingyong Miao, Fangchao Yuan
Summary: The study investigates the role of the p53/miR-34a/SIRT1 positive feedback loop in the termination of liver regeneration and its potential relationship with liver cancer. The overexpression of p53 or miR-34a terminates liver regeneration early and enhances the proapoptotic effect of the positive feedback loop. Additionally, the positive feedback loop is inhibited in hepatocellular carcinoma (HCC) patients with P53 mutations.
Article
Multidisciplinary Sciences
Taryn B. Hogan, Nivedita Tiwari, M. R. Nagaraja, Shwetha K. Shetty, Liang Fan, Rashmi S. Shetty, Yashodhar P. Bhandary, Sreerama Shetty
Summary: Idiopathic pulmonary fibrosis (IPF) is a life-threatening disease caused by abnormal repair responses to lung injury. The expression of miR-34a and its regulation of p53 have been found to play a role in reducing fibrotic markers in fLfs. Increasing the expression of miR-34a can reduce the severity of lung fibrosis. Furthermore, treating fLfs with CSP or CSP7 can restore miR-34a expression and reduce expression of fibrotic markers.
Article
Biochemistry & Molecular Biology
Yiran Liang, Hong Liu, Jiaming Zhu, Nana Song, Zhihui Lu, Yi Fang, Jie Teng, Yan Dai, Xiaoqiang Ding
Summary: The study demonstrates that miR-34a activates the p53 signaling pathway to directly inhibit SIRT1, forming a positive feedback loop that contributes to podocyte injury in diabetic nephropathy. This plays a critical role in the pathogenesis of diabetic kidney disease.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2021)
Article
Immunology
Laura A. Ridgley, Jonathan Caron, Angus Dalgleish, Mark Bodman-Smith
Summary: The expression of activatory and inhibitory receptors on V gamma 9V delta 2 T-cells was assessed to explore the potential regulation of their activity. The results showed that V gamma 9V delta 2 T-cells expressed high levels of activatory markers and variable levels of inhibitory receptors, which were upregulated upon stimulation. However, immune checkpoint blockade had no effect on the cytotoxic capacity or cytokine production of V delta 2+ T-cells when cultured with tumor cells expressing cognate ligands.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Oncology
Li-Juan Pei, Peng-Jun Sun, Kui Ma, Yan-Yan Guo, Ling-Yan Wang, Fei-De Liu
Summary: SNHG7 is upregulated in gastric cancer and correlates with cisplatin resistance, while miR-34a is downregulated and enhances sensitivity to cisplatin-resistant cells. The negative association between SNHG7 and miR-34a suggests a potential regulatory mechanism for cisplatin resistance in gastric cancer.
Article
Multidisciplinary Sciences
Shantanu Gupta, Pritam Kumar Panda, Ronaldo F. Hashimoto, Shailesh Kumar Samal, Suman Mishra, Suresh Kr Verma, Yogendra Kumar Mishra, Rajeev Ahuja
Summary: Transfection of tumor suppressor miRNAs, such as miR-34a, miR-449a, and miR-16, can regulate apoptosis, senescence, and autophagy in cancer cells. However, the specific functions of miR-34a and miR-449a in autophagy and the cooperative or individual roles of these three miRNAs in the functional G1/S checkpoint signaling pathways in HeLa cells remain unknown. This study presents a synthetic Boolean network illustrating the regulatory effects of these miRNAs and demonstrates their advanced role in cervical cancer signaling pathways.
SCIENTIFIC REPORTS
(2022)
Article
Medicine, Research & Experimental
Qiuxia Li, Quanjiang Zhang
Summary: MicroRNAs (miRNAs) are small endogenous RNAs that regulate gene expression by binding to the mRNAs of protein-coding genes. In endothelial cells, miR-34a is an early identified miRNA that plays important roles in regulating endothelial functions, angiogenesis, differentiation, senescence, inflammatory response, responses to shear stress, and mitochondrial function. This review provides an overview of the current understanding of miR-34a in endothelial biology and discusses its potential as a therapeutic target for vascular diseases.
Article
Biochemistry & Molecular Biology
Zekai Huang, Markus Kaller, Heiko Hermeking
Summary: miR-34a and miR-34b/c, as direct targets of p53, play a crucial role in the tumor suppressive effects of p53. Inactivating miR-34a and/or miR-34b/c in colorectal cancer cell line HCT116 had significant effects on proliferation, migration, invasion, chemosensitivity, autophagy, and apoptosis. The concomitant deletion of miR-34a and miR-34b/c resulted in EMT signature enrichment, impaired gene repression by the p53-DREAM pathway, and elevated autophagy. A gene signature upregulated in cells with combined inactivation of miR-34a and miR-34b/c was associated with invasive colon cancer subtype CMS4, poor overall survival in CRC patients, and 5-FU resistance in CRC cell lines.
CELL DEATH AND DIFFERENTIATION
(2023)
Article
Biochemistry & Molecular Biology
Jiaying Fu, Sihang Yu, Xiyao Zhao, Chaoke Zhang, Luyan Shen, Yanan Liu, Huimei Yu
Summary: The metabolism and apoptosis of tumor cells are important for their sensitivity to chemotherapeutic drugs. In this study, the combined treatment of p53 and cisplatin was found to inhibit mitochondrial function, promote mitochondrial pathway-induced apoptosis, and increase sensitivity. The expression of TIGAR, a regulator of cellular metabolism, was also inhibited after the combined treatment. These findings suggest that TIGAR may serve as a potential therapeutic target to increase the sensitivity of lung cancer cells to cisplatin.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)