Journal: Cancers

Article Title: Acid Adaptation Promotes TRPC1 Plasma Membrane Localization Leading to Pancreatic Ductal Adenocarcinoma Cell Proliferation and Migration through Ca 2+ Entry and Interaction with PI3K/CaM

doi: 10.3390/cancers14194946

Figure Lengend Snippet: TRPC1 silencing decreases the expression of CDK6, -1, -2, and cyclin A and increases the expression of p21 CIP1 to a greater extent in acid recovery conditions. ( A ) Western blot analysis of relevant cyclin-dependent kinase complexes and cyclins and their inhibitor p21 CIP1 from cells grown under acid adaptation (6.5) or acid recovery conditions (7.4R). ( B ) Quantification of Western blot analysis representing the expression of CDK6, ( C ) CDK2, ( D ) CDK1, ( E ) cyclin A, and ( F ) p21 CIP1 in siTRPC1 lysates compared to siCTRL lysates from PANC-1 cells grown under acid adaptation (6.5) or acid recovery (7.4R) conditions ( n = 3 − 6). Welch’s correction t -test was used to determine the significant difference between siCTRL and siTRPC1. *, **, and *** indicate p < 0.05, 0.01, and 0.001, respectively. The uncropped blots are shown in .

Article Snippet: The primary antibodies used were: anti-TRPC1 (1:1000, Abcam, Waltham, MA, USA), anti-GAPDH (1:2000, Cell Signaling Tech., Danvers, MA, USA), anti-CDK6 (1:500, Cell Signaling Tech., Danvers, MA, USA), anti-Cyclin A (1:500, Santacruz Biotechnology, Dallas, TX, USA), anti-CDK2 (1:500, Cell Signaling Tech., Danvers, MA, USA), anti-CDK1 (1:500, Cell Signaling Tech., Danvers, MA, USA), anti-p21 CIP1 (1:500, Cell Signaling Tech., Danvers, MA, USA), anti-PI3K p85α (1:500, Bioworld Technology, tebu-bio, France), anti-calmodulin (1:500, Santacruz Biotechnology, Dallas, TX, USA), anti-pAKT (Ser473) (1:500, Cell Signaling Tech., Danvers, MA, USA), anti-AKT (1:500, Cell Signaling Tech., Danvers, MA, USA), anti-pERK1/2 (Thr202/Tyr204) (1:500, Cell Signaling Tech., Danvers, MA, USA), and anti-ERK1/2 (1:500, Cell Signaling Tech., Danvers, MA, USA).

Techniques: Expressing, Western Blot

Journal: Medical oncology (Northwood, London, England)

Article Title: ELK1-induced up-regulation of KIF26B promotes cell cycle progression in breast cancer.

doi: 10.1007/s12032-021-01607-6

Figure Lengend Snippet: Fig. 6 KIF26B promotes cell proliferation by modulated the levels of cell cycle-related proteins in MDA-MB-231 and MDA-MB-468 cells. A Western blot analysis showed that the expression levels of Wnt, β-catenin, c-Myc, cyclinD1, CDK4, p-Rb decreased, and p27 increased in both MDA-MB-231 cells and MDA-MB-468 cells after KIF26B silencing, while cyclin E1, CDK2, CDK6, p53, and p21 remained unchanged. B Proposed functional action of KIF26B in regulating BC tumo- rigenesis. The transcriptional factor ELK1 promoted KIF26B expression by directly binding to its core promoter region, and KIF26B acted on the Wnt/β- catenin signaling pathway to up-regulate c-Myc and regulate the cell cycle-related protein expression levels, including cyc- lin D1, CDK4, p-Rb, and p27 to promote cell cycle progression

Article Snippet: The primary antibodies used were as follows: KIF26B (1:500, 17422–1-AP, Proteintech), ELK1 (1:500, ab32106, Abcam), Wnt6 (1:1500, ab50030, Abcam), GAPDH (1:1,000, #5174, CST), β-catenin (1:2,000, ab32532, Abcam), c-Myc (1:1,000, #18583, CST), cyclin D1 (1:1,000, #55506, CST), CDK4 (1:1,000, #12790, CST), p27 (1:1,000, #3686, CST), cyclin E1 (1:1000, #20808, CST), CDK2 (1:1,000, #18048, CST), p21 (1:1,000, #2947, CST, CDK6 (1:1000, #13331, CST), p53 (1:1000, #9282, CST), p-Rb (1:1000, #8516, CST).

Techniques: Western Blot, Expressing, Functional Assay, Binding Assay

Journal: Oncotarget

Article Title: TLR4 interaction with LPS in glioma CD133+ cancer stem cells induces cell proliferation, resistance to chemotherapy and evasion from cytotoxic T lymphocyte-induced cytolysis

doi: 10.18632/oncotarget.18586

Figure Lengend Snippet: Expression of CDK4, CDK6, cyclin E, bcl-2, NF-κB, phosphorylated p38, p38, phosphorylated JNK, JNK, phosphorylated ERK, ERK, phosphorylated Akt, Akt, and β-actin in glioma CD133+ CSCs isolated from CSCs generated from SF295 after stimulation with LPS (1 μg/mL) at different time points (0 hours to 6 days).

Article Snippet: Phosphorylated Akt, Akt, bcl-2, survivin, BAX, CDK4, CDK6, and cyclin E monoclonal antibodies were purchased from Cell Signaling Technology (Beverly, USA).

Techniques: Expressing, Isolation, Generated

Journal: Oncotarget

Article Title: JQ1 suppresses tumor growth via PTEN/PI3K/AKT pathway in endometrial cancer

doi: 10.18632/oncotarget.11631

Figure Lengend Snippet: Six endometrial cancer cell lines were cultured for 24 hours and then treated with JQ1 at indicated doses in 96 well plates for 72 hours. ( A ) Cell proliferation was assessed by MTT assay. ( B ) JQ1 (100 nM) notably suppressed the colon formation in Hec-1a and KLE cells ( p = 0.009 and 0.021 respectively). ( C ) JQ1 induced significant G1 phase arrest in Hec-1a and KLE cells after 24 hours of treatment with JQ1 (ranged from 0 nM to 1000 nM, p = 0.015 and 0.032 respectively). ( D ) In a time-lapse course, microarray analysis showed that JQ1 (500 nM) notably downregulated the mRNA expression of c-Myc, cyclin D1 and CDK4 in Hec-1a cells. ( E ) Western blotting results indicated that JQ1 inhibited cyclin D, CDK2, CDK4, CDK6 and cyclin E expression in a dose dependent manner after 24 hours of treatment. ( F ) JQ1 induced Annexin V expression in Hec-1a and KLE cells after 24 hours of treatment.

Article Snippet: All the primary antibodies for phosphorylated-S6, pan-S6, phosphorylated-AKT, pan-AKT, cyclin D1, CDK6, CDK4 and Ki-67 were obtained from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Cell Culture, MTT Assay, Microarray, Expressing, Western Blot