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1 sembly and increases migratory propensity in renal cancer cells.
2 tion of Akt kinase activity in both types of renal cancer cells.
3 tly inhibited IGF-1R-driven proliferation of renal cancer cells.
4 tate, breast, lung, bladder, colorectal, and renal cancer cells.
5 er473 in response to NVP-BEZ235 treatment in renal cancer cells.
6  pathway induces HO-1 to promote survival of renal cancer cells.
7 colony formation, migration, and invasion in renal cancer cells.
8  c-Met phosphorylation and Ras activation in renal cancer cells.
9 in vivo in human prostate, breast, lung, and renal cancer cells.
10 e mRNA stability of VEGF in 786-0 and Caki-1 renal cancer cells.
11 iR-23b was knocked down by its antagomirs in renal cancer cells.
12 th, invasion, and inhibition of apoptosis in renal cancer cells.
13 expression using siRNA promoted apoptosis of renal cancer cells.
14 rough modulation of TIS11B protein levels in renal cancer cells.
15 ited CNI-mediated augmented proliferation of renal cancer cells.
16 oth HIF1alpha and HIF2alpha in VHL-deficient renal cancer cells.
17 has been shown to reverse tumorigenesis with renal cancer cells.
18 gulatory component of HIFalpha expression in renal cancer cells.
19 poptosis induced by serum deprivation in the renal cancer cells.
20 ary and sufficient to suppress E-cadherin in renal cancer cells.
21                                     In human renal cancer cells (786-0 and Caki-1) and renal epitheli
22 uld induce HO-1, and promote the survival of renal cancer cells (786-0 and Caki-1).
23 uman normal renal epithelial cells (REC) and renal cancer cells (786-0 and Caki-1).
24 well as endogenous TRPC1:C4 channels in A498 renal cancer cells, all with low micromolar IC(50) value
25                         FILNC1 deficiency in renal cancer cells alleviates energy stress-induced apop
26 or tyrosine kinase c-Met is overexpressed in renal cancer cells and can play major role in the growth
27 -A*0201-restricted antigen expressed by both renal cancer cells and normal kidney cells.
28 ur data signify that HO-1 is up-regulated in renal cancer cells as a survival strategy against chemot
29  overexpressed HO-1 promotes the survival of renal cancer cells by inhibiting cellular apoptosis; we
30  apoptosis and immune escape mechanism(s) of renal cancer cells by the regulations of novel molecules
31 ent, were found to induce HO-1 expression in renal cancer cells Caki-1 and 786-O; and the apoptotic e
32  that the overexpression of CXCR3-B in human renal cancer cells (Caki-1) promoted cellular apoptosis
33 issues; and the overexpression of CXCR3-B in renal cancer cells can significantly inhibit cell prolif
34 essed the migration of aggressive clear cell renal cancer cell carcinoma cell lines.
35 y and metastatic clonally-related clear cell renal cancer cells (ccRCC) grown in physiological media
36 e phenotypes of isogenic pairs of clear cell renal cancer cells (ccRCC), with or without VHL, upon th
37  in increased proliferation and migration of renal cancer cells; CNI-mediated cell proliferation invo
38            Increased expression of IGF-1R in renal cancer cells correlates with their potency of tumo
39 uced and HO-1-mediated pathway could protect renal cancer cells from apoptosis.
40      Functionally, PIK3R3 depletion promotes renal cancer cell growth and orthotopic tumor growth whi
41               Therefore, Jade-1 may suppress renal cancer cell growth in part by increasing apoptosis
42                             Jade-1 inhibited renal cancer cell growth, colony formation, and tumor fo
43                  Interestingly, FH-deficient renal cancer cells had low surface expression of ULBP2/5
44 reduced cyclinD1, and arrested the growth of renal cancer cells in G1/S phase.
45  inhibits the growth of FLCN-deficient human renal cancer cells in mouse xenografts.
46 to block proliferation and invasion of 786-O renal cancer cells in vitro.
47                          Interestingly, like renal cancer cells, in AsPC-1 cells PKC-zeta leads to di
48                      VHL reintroduction into renal cancer cells increases endogenous Jade-1 protein a
49 n of IGF-1R levels and miR-214 expression in renal cancer cells independent of VHL status.
50 e we report that prostaglandin E(2) promotes renal cancer cell invasion through a signal transduction
51 croRNA hsa-miR-29b in the VHL-overexpressing renal cancer cell line 786-O.
52  of apoptotic cells in the sFRP3-transfected renal cancer cell line A498.
53     We isolated a clone (R331) of the murine renal cancer cell line Renca that was strikingly more se
54 ine NCI/ADR-RES (GI(5)(0) = 0.0169 muM), and renal cancer cell line RXF 393 (GI(5)(0) = 0.0197 muM).
55 pproach for treatment follow-up, utilizing a renal cancer cell line with rapamycin as a tool compound
56 n-6, was recently described to be present in renal cancer cell lines and fetal kidney, but no data on
57 n of miR-205 was significantly suppressed in renal cancer cell lines and tumors when compared with no
58 helial cells, human renal cancer tissues and renal cancer cell lines demonstrated higher expression o
59 signaling responses in vitro in prostate and renal cancer cell lines in a dose-dependent manner.
60   Knockdown of galectin-1 gene expression in renal cancer cell lines reduced cell invasion, clonogeni
61                                 Three of six renal cancer cell lines tested revealed MN expression.
62 pression was barely detectable in all tested renal cancer cell lines, regardless of VHL status.
63 or activity against human breast, colon, and renal cancer cell lines, undergoes hydrolysis in aqueous
64 lation was confirmed in three additional VHL-renal cancer cell lines, was insensitive to the prolyl h
65 lective inhibitor of the growth of six human renal cancer cell lines.
66 e role of sFRP3 using primary and metastatic renal cancer cell lines.
67 d aid investigators in analysing appropriate renal cancer cell lines.
68 uced AKT Ser473 phosphorylation and rendered renal cancer cells more susceptible to NVP-BEZ235-mediat
69 olonged the survival of mice inoculated with renal cancer cells or T24 human bladder cancer cells.
70                   The effect of rapamycin on renal cancer cell phenotype, molecules (E-cadherin, p27
71 e report that VHL-deficient and VHL-positive renal cancer cells possess significantly decreased level
72 ence for a novel mechanism for IGF-1R-driven renal cancer cell proliferation involving miR-214 and mT
73  miR-214 significantly blocked IGF-1R-forced renal cancer cell proliferation, which was reversed by e
74 olimus, and the effect of treatment on mouse renal cancer cell pulmonary metastasis was investigated.
75  (expressing PD-L1 receptor PD-1) and murine renal cancer cells (RENCA, expressing high PD-L1).
76  HIF2alpha expression is dependent on PLD in renal cancer cells suggests that targeting PLD signals m
77                                           In renal cancer cells, the inactivation of the tumor suppre
78 that l-2HG remodels amino acid metabolism in renal cancer cells through combined effects on histone m
79 he translocation behaviors of the metastatic renal cancer cells through plain and nanotextured PDMS m
80 n, migration, EMT and stem-like phenotype in renal cancer cells through the AKT/GSK3beta/CTNNB1 pathw
81 hich c-Met can promote increased survival of renal cancer cells through the regulation of HO-1 and PD
82 ary ccRCC, as a crucial event for metastatic renal cancer cells to acquire the capability to generate
83                    Here, we used 786-0 human renal cancer cells to investigate the effect of cyclospo
84                    Rapamycin conditioning of renal cancer cells upregulated E-cadherin expression and
85                             Proliferation of renal cancer cells was suppressed by miR-205, mediated b
86                                        Using renal cancer cells, we confirmed that stauprimide inhibi
87 expression of any apoptosis-related genes in renal cancer cells, we performed a protein array.
88           In a xenograft model wherein, live renal cancer cells were implanted under the kidney capsu
89 etic conditions was also dependent on PLD in renal cancer cells with restored pVHL expression.