Carbonic anhydrase inhibitor suppresses invasion of renal cancer cells in vitro

Epacadostat (EPA), a selective indoleamine-2,3-dioxygenase 1 (IDO1) inhibitor, has been investigatedin vitroas a human (h) Carbonic Anhydrase Inhibitor (CAI).

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Effects of Cytokines on Clonogenic Growth of Primary Renal Cancer Cells: An in vitro Phase II Study

Oncology Research and Treatment ◽

10.1159/000217348 ◽

1992 ◽

Vol 15 (2) ◽

pp. 147-150 ◽

Cited By ~ 4

Author(s):

A.-R. Hanauske ◽

W. De Riese ◽

M. Joraschkewitz ◽

M. Freund ◽

H. Poliwoda

Keyword(s):

Cancer Cells ◽

Renal Cancer ◽

Phase Ii ◽

Phase Ii Study ◽

Clonogenic Growth

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MP73-10 RITONAVIR, A POTENT INHIBITOR OF CYP3A4, ENHANCES THE ANTICANCER EFFECTS OF ENTINOSTAT IN RENAL CANCER CELLS IN VITRO AND IN VIVO

The Journal of Urology ◽

10.1016/j.juro.2017.02.3355 ◽

2017 ◽

Vol 197 (4S) ◽

Author(s):

Takako Asano ◽

Akinori Sato ◽

Kazuki Okubo ◽

Makoto Isono ◽

Tomohiko Asano

Keyword(s):

Cancer Cells ◽

Renal Cancer ◽

Potent Inhibitor ◽

Anticancer Effects

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An in-vitro tumour microenvironment model using adhesion to type I collagen reveals Akt-dependent radiation resistance in renal cancer cells

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfp525 ◽

2009 ◽

Vol 25 (2) ◽

pp. 373-380 ◽

Cited By ~ 9

Author(s):

Lina Krasny ◽

Nilly Shimony ◽

Keren Tzukert ◽

Raphael Gorodetsky ◽

Shimon Lecht ◽

...

Keyword(s):

Cancer Cells ◽

Renal Cancer ◽

Radiation Resistance ◽

Type I Collagen ◽

Tumour Microenvironment ◽

Type I

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CHLOROTHIAZIDE

PEDIATRICS ◽

10.1542/peds.22.2.236 ◽

1958 ◽

Vol 22 (2) ◽

pp. 236-237

Author(s):

JOHN D. CRAWFORD

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Carbonic Anhydrase ◽

Renal Insufficiency ◽

Chronic Renal Insufficiency ◽

Free Water ◽

Carbonic Anhydrase Inhibitor ◽

Diuretic Agent

CHLOROTHIAZIDE is a new, orally effective diuretic agent chemically related to acetazolamide. Curiously, it is a considerably less potent carbonic anhydrase inhibitor, at least in vitro and, in vivo, its effect has been found additive to that of acetazolamide as it is to the action of the mercurials. Laragh's observations suggest that chlorothiazide inhibits the process of solute reabsorption which normally gives rise to "free" water in the urine. Thus, it may well have a locus of action in the kidney different from that of its chemical cousin or the mercury derivities. There have been optimistic reports of its efficacy in a variety of edema states including nephrosis, cirrhosis of the liver, congestive heart failure, acute hemorrhagic nephritis and chronic renal insufficiency.

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Cell-cycle arrest and senescence in TP53-wild type renal carcinoma by enhancer RNA-P53-bound enhancer regions 2 (p53BER2) in a p53-dependent pathway

Cell Death and Disease ◽

10.1038/s41419-020-03229-8 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Haibiao Xie ◽

Kaifang Ma ◽

Kenan Zhang ◽

Jingcheng Zhou ◽

Lei Li ◽

...

Keyword(s):

Cell Cycle ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Cell Lines ◽

Kidney Cancer ◽

Renal Cancer ◽

Wild Type ◽

Enhancer Rna ◽

Cycle Arrest

AbstractTP53 is a classic tumor suppressor, but its role in kidney cancer remains unclear. In our study, we tried to explain the role of p53 in kidney cancer through the p53-related enhancer RNA pathway. Functional experiments were used to explore whether P53-bound enhancer regions 2 (p53BER2) has a role in the cell cycle and senescence response of TP53-wild type (WT) renal cancer cells in vitro or vivo. RNA-sequencing was used to identify the potential target of p53BER2. The results showed that the expression level of P53BER2 was downregulated in renal cancer tissues and cell lines, further dual-luciferase experiments and APR-256-reactivated experiments showed p53BER2 expresses in a p53-dependent way. Moreover, knockdown p53BER2 could reverse nutlin-3-induced cytotoxic effect in TP53-WT cell lines. Further exploration showed the downregulation of p53BER2 could reverse nutlin-3-induced G1-arrest and senescence in TP53-WT cell lines. What is more, the knockdown of p53BER2 showed resistance to nutlin-3 treatment in vivo. Additionally, we found BRCA2 could be regulated by p53BER2 in vitro and vivo; further experiment showed p53BER2 could induce cell-cycle arrest and DNA repair by mediating BRCA2. In summary, the p53-associated enhancer RNA-p53BER2 mediates the cell cycle and senescence of p53 in TP53-WT renal cancer cells.

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Cancer Associated Fibroblasts Promote Renal Cancer Progression Through a TDO/Kyn/AhR Dependent Signaling Pathway

Frontiers in Oncology ◽

10.3389/fonc.2021.628821 ◽

2021 ◽

Vol 11 ◽

Author(s):

Li-bo Chen ◽

Shun-ping Zhu ◽

Tian-pei Liu ◽

Heng Zhao ◽

Ping-feng Chen ◽

...

Keyword(s):

Cancer Cells ◽

Renal Cancer ◽

Cancer Progression ◽

Cancer Associated Fibroblasts ◽

Aromatic Hydrocarbon Receptor ◽

Cancer Migration ◽

Tumor Tissues ◽

Enhanced Secretion

Cancer associated fibroblasts (CAFs) play crucial roles in cancer development, however, the specific mechanisms of CAFs associated renal cancer progression remain poorly understood. Our study observed enriched CAFs in high degree malignant tumor tissues from renal cancer patients. These CAFs isolated from tumor tissues are prone to facilitate drugs resistance and promote tumor progression in vitro and in vivo. Mechanistically, CAFs up-regulated tryptophan 2, 3-dioxygenase (TDO) expression, resulting in enhanced secretion of kynurenine (Kyn). Kyn produced from CAFs could up-regulated the expression of aromatic hydrocarbon receptor (AhR), eventually resulting in the AKT and STAT3 signaling pathways activation. Inhibition of AKT signal prevented cancer cells proliferation, while inhibition of the STAT3 signal reverted drugs resistance and cancer migration induced by kynurenine. Application of AhR inhibitor DMF could efficiently suppress distant metastasis of renal cancer cells, and improve anticancer effects of sorafenib (Sor)/sunitinib (Sun), which described a promising therapeutic strategy for clinical renal cancer.

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Cell cycle arrest and senescence in P53-wild type renal carcinoma by enhancer RNA - P53-bound enhancer regions 2(p53BER2) through p53-dependent pathway

10.21203/rs.3.rs-22612/v1 ◽

2020 ◽

Author(s):

HAIBIAO XIE ◽

Kaifang Ma ◽

Kenan Zhang ◽

Jingcheng Zhou ◽

Lei Li ◽

...

Keyword(s):

Cell Cycle ◽

Cancer Cells ◽

Cell Lines ◽

Kidney Cancer ◽

Renal Cancer ◽

G1 Arrest ◽

Wild Type ◽

Enhancer Rna

Abstract Background P53 is a classic tumor suppressor, but its role in kidney cancer remains unclear. In our study, we tried to explain the role of p53 in kidney cancer through p53 enhancer RNA-related pathway. Methods qPCR and luciferase reporters were used to detect the expression of p53-related enhancer RNA. Nutlin3 and artificial "microRNA" were used to induce and inhibit the expression of p53 enhancer RNA, respectively. Cycle analysis and β-galactosidase assay were used to explore whether P53-bound enhancer regions 2(p53BER2) plays a role in the cell cycle and senescence response of p53-wild type (WT) renal cancer cells. The function of p53BER2 was further analyzed in vivo by nude mice. RNA sequencing was used to identify the potential target of p53BER2. Results The results showed that P53BER2 expression was down-regulated in renal cancer tissues and cell lines and could specifically express in p53-WT renal cancer cell lines. Knockdown p53BER2 could reverse nutlin-3-induced cytotoxic effect in p53-WT cell lines. Further, downregulation of p53BER2 could reverse nutlin-3-induced G1 arrest and senescence in p53-WT cell lines. What is more, knockdown of p53BER2 showed a resistance to nutlin-3 treatment in Vivo. Additionally, we found BRCA2 could be regulated by p53BER2 in vitro and vivo, which suggested BRCA2 might mediate the function of p53BER2 in RCC. Conclusions The p53-associated enhancer RNA-p53BER2 mediates the cell cycle and senescence of p53 in p53-WT renal cancer cells. This further provides a novel approach and insight for the RCC and p53 research in renal cancer.

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