Down-regulation of CD74 inhibits growth and invasion in clear cell renal cell carcinoma through HIF-1α pathway

Ji, Shou‐Ping; Su, Xiaolin; Cheng, Wenlong; Zhang, Haijian; Zhao, Yuqian; Han, Zhixing

doi:10.1016/j.urolonc.2012.09.013

Cited by 17 publications

(19 citation statements)

References 27 publications

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“…Consequently, exploring the inherent molecular mechanism for diagnosing and treating KIRC needed urgent resolution. 5'-AUAGUGAAUUAAGCUUCGCGAGUUAUAG-3' such as the synthetic contribution of hypoxia inducible factor 1 (HIFlα) and CD74 to inhibiting KIRC cells' growth and invasion, 26 and the independently predictive role of DHH for KIRC prognosis. 27 In this investigation, MALAT1 was observed to differentially express within KIRC tissues and adjacent normal tissues, manifesting that this lncRNA potentially marked the onset and progression of KIRC ( Figure 1).…”

Section: Acvr2b Was Targeted By Mir-194-5p In Kirc Cellsmentioning

confidence: 99%

LncRNA MALAT1 modified progression of clear cell kidney carcinoma (KIRC) by regulation of miR‐194‐5p/ACVR2B signaling

Zhang

Chen

et al. 2018

Molecular Carcinogenesis

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This investigation was purposed to extrapolate whether and how lncRNA MALAT1, miR‐194‐5p, and ACVR2B altered development of clear cell kidney carcinoma (KIRC). We totally gathered 318 pairs of KIRC tissues and adjacent normal tissues, and also purchased human KIRC cell lines and normal human proximal tubular epithelial cell line. Besides, si‐MALAT1, pcDNA‐MALAT1, miR‐194‐5p mimic, miR‐194‐5p inhibitor, and negative control (NC) were, respectively, transfected into KIRC cells. The viability, proliferation, and apoptosis of the cells were determined with CCK‐8 assay, colony formation assay, and flow cytometry. Dual‐luciferase reporter gene assay was implemented to validate the targeted relationships between MALAT1 and miR‐194‐5p, as well as between miR‐194‐5p and ACVR2B. The results showed that highly expressed MALAT1, ACVR2B, and lowly expressed miR‐194‐5p were associated with larger tumor size (≥4 cm), advanced TNM stage and poor prognosis of KIRC patients, when, respectively, compared with lowly expressed MALAT1, ACVR2B, and highly expressed miR‐194‐5p (P < 0.05). Transfection of pcDNA‐MALAT1, miR‐194‐5p inhibitor, and pcDNA‐ACVR2B conferred the KIRC cells with promoted viability and proliferation, as well as reduced apoptosis (P < 0.05). Treatment of rats with pcDNA‐MALAT1, miR‐194‐5p inhibitor, or pcDNA‐ACVR2B also contributed to larger tumor size growing in them (P < 0.05). Moreover, MALAT1 could directly target miR‐194‐5p to suppress its expression, and ACVR2B was the targeted molecule of miR‐194‐5p (P < 0.05). Finally, ACVR2B could reverse the effects exerted by miR‐194‐5p on viability, proliferation, and apoptosis of KIRC cells (P < 0.05). In conclusion, LncRNA MALAT1/miR‐194‐5p/ACVR2B signaling was regarded as a candidate pathway for modulating KIRC progression.

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Section: Acvr2b Was Targeted By Mir-194-5p In Kirc Cellsmentioning

confidence: 99%

LncRNA MALAT1 modified progression of clear cell kidney carcinoma (KIRC) by regulation of miR‐194‐5p/ACVR2B signaling

Zhang

Chen

et al. 2018

Molecular Carcinogenesis

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“…Absence of CD44 or the terminal differentiation state of podocytes may account for the differences. MIF, MIF-2, CD74, and CD44 promote clear cell renal cell carcinoma, cell proliferation, and HIF-activation ( 38 , 39 ). While MIF and MIF-2 overlap in controlling cell survival and tumor formation, MIF-2 plays a dominant role in renal cancer tumor growth in vivo ( 40 ).…”

Section: Cd74mentioning

confidence: 99%

CD74 in Kidney Disease

et al. 2015

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CD74 (invariant MHC class II) regulates protein trafficking and is a receptor for macrophage migration inhibitory factor (MIF) and d-dopachrome tautomerase (d-DT/MIF-2). CD74 expression is increased in tubular cells and/or glomerular podocytes and parietal cells in human metabolic nephropathies, polycystic kidney disease, graft rejection and kidney cancer and in experimental diabetic nephropathy and glomerulonephritis. Stressors like abnormal metabolite (glucose, lyso-Gb3) levels and inflammatory cytokines increase kidney cell CD74. MIF activates CD74 to increase inflammatory cytokines in podocytes and tubular cells and proliferation in glomerular parietal epithelial cells and cyst cells. MIF overexpression promotes while MIF targeting protects from experimental glomerular injury and kidney cysts, and interference with MIF/CD74 signaling or CD74 deficiency protected from crescentic glomerulonephritis. However, CD74 may protect from interstitial kidney fibrosis. Furthermore, CD74 expression by stressed kidney cells raises questions about the kidney safety of cancer therapy strategies delivering lethal immunoconjugates to CD74-expressing cells. Thus, understanding CD74 biology in kidney cells is relevant for kidney therapeutics.

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“…CD74, first identified as a chaperone of major histocompatibility complex (MHC) class II proteins in antigen presentation for the immune response, was subsequently found to be a receptor of macrophage migration inhibitory factor (MIF) that was actively involved in various autoimmune and inflammatory disorders as well as tumorigenesis [62,63]. Recent data have shown that CD74 protein is upregulated in cancer cells, indicating its role in carcinogenesis and angiogenesis [63][64][65][66].…”

Section: Cd74mentioning

confidence: 99%

“…Recent data have shown that CD74 protein is upregulated in cancer cells, indicating its role in carcinogenesis and angiogenesis [63][64][65][66]. Moreover, it is well known that there is a close link between chronic inflammation and malignancies, which could be initiated by recruitment of inflammatory cells and production of inflammatory mediators.…”

Section: Cd74mentioning

confidence: 99%

Prognostic value of several biomarkers for the patients with malignant pleural mesothelioma

Liu

Jiao

et al. 2015

Tumor Biol.

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Malignant pleural mesothelioma (MPM) is a highly aggressive tumor of the pleura closely related to asbestos exposure. Rare as it is, the incidence of MPM is predicted to increase mainly as a result of a lengthy latency period from the initial asbestos exposure, making it a public health concern for the next decades. Moreover, the patients with MPM have an extremely poor prognosis due to its high resistance to conventional oncologic treatments and delayed diagnosis. Although the result of current therapeutic modalities based on patient features and clinical stages is very frustrating, great advances have been shown in the knowledge of molecular biology of MPM in recent years. This is accompanied by dozens of putative prognostic biomarkers that are actively involved in tumor biological activities. These prognostic candidates can offer us a new insight into the biological characteristics of MPM, contributing to development of individualized therapeutic strategies directed against oncogenesis and tumor progression. Thus, personalized approaches based on the molecular biology of the patient's tissue or body fluid will potentially improve the present disappointing outcome, bringing new hope for patients with MPM. This article reviews the principal and several novel biomarkers that can have an influence on prognosis, in the hope that they can provide us with a more profound understanding of the biology of this lethal disease.

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Down-regulation of CD74 inhibits growth and invasion in clear cell renal cell carcinoma through HIF-1α pathway

Cited by 17 publications

References 27 publications

LncRNA MALAT1 modified progression of clear cell kidney carcinoma (KIRC) by regulation of miR‐194‐5p/ACVR2B signaling

LncRNA MALAT1 modified progression of clear cell kidney carcinoma (KIRC) by regulation of miR‐194‐5p/ACVR2B signaling

CD74 in Kidney Disease

Prognostic value of several biomarkers for the patients with malignant pleural mesothelioma

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