PTB-independent ShcA pools require Src to promote mammary tumorigenesis. PTB-independent ShcA pools require Src to promote mammary tumorigenesis. A, Src.

Slides:

Advertisements

Similar presentations

PP1 and PP2A inhibitors rescue α-SMA expression and Akt phosphorylation from the inhibitory effects of TSA. After serum starvation, NHLFs were pretreated.

Advertisements

Pirh2 promotes p73 ubiquitination in vivo.

Level of EGFR inhibition determines cell death response in EGFR mutant GBM cells. Level of EGFR inhibition determines cell death response in EGFR mutant.

DAO enhances DNA damage–induced ROS accumulation, cooperating with PRODH. DAO enhances DNA damage–induced ROS accumulation, cooperating with PRODH. (A)

SGK3 Mediates INPP4B-Dependent PI3K Signaling in Breast Cancer

Volume 6, Issue 2, Pages (August 2004)

Imipramine and promethazine induce the apoptotic cell death of SCLC cells through activation of caspase-3. Imipramine and promethazine induce the apoptotic.

Volume 50, Issue 2, Pages (April 2013)

Anti-CD96 combines with anti–CTLA-4 or anti–PD-1 to suppress experimental and spontaneous lung metastases. Anti-CD96 combines with anti–CTLA-4 or anti–PD-1.

AKT2, but not AKT1, is required for regulating survival of PTEN-deficient prostate tumor spheroids. AKT2, but not AKT1, is required for regulating survival.

Pharmacologic inhibition of eIF5A hypusination sensitizes KRas-driven tumor cells to MEK and KRas inhibition. Pharmacologic inhibition of eIF5A hypusination.

Combined HDAC and mTOR inhibitors kill NF1-mutant malignancies in vitro and in vivo. Combined HDAC and mTOR inhibitors kill NF1-mutant malignancies in.

IL-6 signaling affects response to erlotinib in head and neck (HNSCC) cells. IL-6 signaling affects response to erlotinib in head and neck (HNSCC) cells.

Expression of p110γ isoform in macrophages promotes tumor growth and angiogenesis. Expression of p110γ isoform in macrophages promotes tumor growth and.

Protection from 4T1 tumor rechallenge in treated mice.

Curcumin-generated ROS activates Chk1 and Chk2 kinases.

Oncogenic Ras signaling activates SFKs and promotes CDCP1-dependent invasion in 3-dimensional (3D) collagen raft culture of HCK. A, HCK1T-E cells, HCK1T-E.

Gramicidin A (GA) decreases HIF protein expression in RCC cells.

PTENP1 serves as a ceRNA in the regulation of tumor growth in RCC

PTENP1 sensitizes renal cancer cells to chemotherapy.

Conversion of CD11bhighCD27high NK cells into MDSCs leads to CD11bhighCD27high and CD11bhighCD27low NK cell reduction. Conversion of CD11bhighCD27high.

Expression profile of RSPO1 and 2 in gastric cancer.

The SFKs confer BRAF inhibitor resistance in BRAF-mutant melanoma cells. The SFKs confer BRAF inhibitor resistance in BRAF-mutant melanoma cells. A, phospho-protein.

A, GP and GR epithelial tumor cells are equally responsive to gefitinib. A, GP and GR epithelial tumor cells are equally responsive to gefitinib. Equal.

Overexpression of Pim kinases contributes to increased protein translation in resistant cells through controlling cap-independent translation. Overexpression.

EGFR and cetuximab sensitivity of SCCUAT

The effect of IAA on tumor growth in an SK-MEL-28 xenograft model.

Effect of G9a on the expression of GSH synthesis enzymes.

Overexpression of DDB2 reduces invasive abilities in lungs of aggressive breast tumor cells. Overexpression of DDB2 reduces invasive abilities in lungs.

Bcl-2 and caspase inhibition fails to inhibit BAMLET-induced cytotoxicity in MCF-7 cells. Bcl-2 and caspase inhibition fails to inhibit BAMLET-induced.

EMT gene expression patterns of M-Wnt and E-Wnt cells in vitro and in vivo. EMT gene expression patterns of M-Wnt and E-Wnt cells in vitro and in vivo.

The antitumor and antimetastatic properties of PF in the MX1 orthotopic model. The antitumor and antimetastatic properties of PF in the.

Fyn cooperates with Src to increase the tumorigenic potential of PTB-independent ShcA signaling complexes. Fyn cooperates with Src to increase the tumorigenic.

Paclitaxel treatment along with CXCR2 knockdown reduces tumor growth and metastasis. Paclitaxel treatment along with CXCR2 knockdown reduces tumor growth.

Targeting HR via CDK inhibition resensitizes recurrent cultures to temozolomide (TMZ). Targeting HR via CDK inhibition resensitizes recurrent cultures.

PTB-independent ShcA pools employ distinct domains to hyperactivate mTOR and Src signaling. PTB-independent ShcA pools employ distinct domains to hyperactivate.

PTB-independent ShcA pools require a functional SH2 domain, but not the tyrosine phosphorylation sites to promote mammary tumorigenesis. PTB-independent.

Combination CDN and PD-L1 mAb treatment of established MOC1 tumors produces consistent tumor rejection. Combination CDN and PD-L1 mAb treatment of established.

Ki-67 expression in M31- and H3-treated tumors (A) and respective Ki-67 labeling indices in the two groups of tumors (B). Ki-67 expression in M31- and.

Localization of oxidated thiols in A375 melanoma cells.

Pirh2 represses p73-dependent transactivation.

GM-CSF is required for CA-MSC–induced tumor metastasis.

NT157 treatment inhibits LNCaP xenograft growth and delays castration-resistant progression. NT157 treatment inhibits LNCaP xenograft growth and delays.

HMQ1611 inhibited breast tumor growth in mice.

Immunophenotypic analysis of TILs in B16 and K1735 melanoma following combination therapy with antibodies targeting PS and PD-1. Immunophenotypic analysis.

Osteoactivin expression is required for the invasive phenotype of in vivo selected bone metastatic 4T1 breast cancer cells. Osteoactivin expression is.

Osteoactivin is overexpressed in aggressively bone metastatic 4T1 subpopulations versus weakly bone metastatic breast cancer populations. Osteoactivin.

Anti-SEMA4D antibody regulates immune-cell infiltration and inhibits growth of Tubo.A5 orthotopic mammary carcinoma. Anti-SEMA4D antibody regulates immune-cell.

The effect of a DIO regimen ± EPA+DHA supplementation on tumor growth.

Combined inhibition of coamplified RTKs is required for response.

Tumor protection induced by therapeutic PLG vaccination in combination with blockade antibodies. Tumor protection induced by therapeutic PLG vaccination.

SPARC is required for spontaneous metastasis

SAHA blocks IR-induced increase of RAD51 protein in MM cells.

Increased expression of angiogenic factors and inflammatory cytokines in mice exposed to hypoxia. Increased expression of angiogenic factors and inflammatory.

AKT activation in HCC2429 is SRC- but not Notch-dependent.

Efficacy of KM100 and/or MTX in BALB/c mice bearing subcutaneous TUBO tumors. Efficacy of KM100 and/or MTX in BALB/c mice bearing subcutaneous TUBO tumors.

The interaction of PALB2 with BRCA1 is required for the assembly of PALB2, BRCA2, and RAD51 nuclear foci. The interaction of PALB2 with BRCA1 is required.

p53β regulates cellular senescence.

Effects of ZOL treatment on pulmonary metastases.

ABT-888 sensitizes multiple ovarian cancer cell lines but not normal cells to FdUrd. ABT-888 sensitizes multiple ovarian cancer cell lines but not normal.

Cabozantinib causes significant tumor cell elimination in vivo, but modest apoptosis induction in vitro. Cabozantinib causes significant tumor cell elimination.

GCS-100 selectively kills KRAS-addicted lung tumors.

AXL-on tumors are heterogeneous for AXL expression and EdU incorporation. AXL-on tumors are heterogeneous for AXL expression and EdU incorporation. A,

Recruitment of CD8+, CD4+, and Foxp3+ cells into oral lesions in response to anti–PD-1 treatment. Recruitment of CD8+, CD4+, and Foxp3+ cells into oral.

T3 or T4 induces MAPK activation in myeloma cells.

Inhibition of HDACs disrupts DNMT1 association with Hsp90.

TAMs upregulate DNMT1 in gastric cancer cells through the CCL5/CCR5/STAT3 pathway. TAMs upregulate DNMT1 in gastric cancer cells through the CCL5/CCR5/STAT3.

I3C reduces the level of Cdc25A protein in breast cancer cells.

SCLC in CMV TKO mice arises from an alternative cell of origin.

Parthenolide inhibits tumor promotion and increases p21 expression in vivo. Parthenolide inhibits tumor promotion and increases p21 expression in vivo.

Presentation transcript:

PTB-independent ShcA pools require Src to promote mammary tumorigenesis. PTB-independent ShcA pools require Src to promote mammary tumorigenesis. A, Src was deleted from ErbB2 mammary epithelial cell line (NMuMG-NeuNT) from the indicated ShcA-expressing cell lines using Crispr/Cas9 genomic editing. Immunoblot analysis of vector control and Src-Crispr (CR) cell lines using Src- and Tubulin-specific antibodies. Vector control and Src-CR of NMuMG-NeuNT ShcAWT (B) and PTBMUT (C) cell lines were injected into the mammary fat pads of immunodeficient mice. The data depict the average treumor volumes (mm3) ± SEM and are representative of 9–10 tumors per group. *, P < 0.05; **, P < 0.01; ****, P < 0.0001. IHC staining of pY416-Src (D) and pS240/244-rS6 (E) in ShcAWTand PTBMUT-expressing NMuMG-NeuNT mammary tumors. The data depict the average positively stained cells or pixels ± SEM is representative of 8–10 tumors per group. **, P < 0.01. F, FLAG immunoprecipitates from indicated cell lines were probed with pY239/240-ShcA or ShcA-specific antibodies via immunoblot analysis. The graph represents densitometric quantification of three independent experiments using ImageJ software. **, P < 0.01. G, Clonogenic assay of specified cell lines treated with DMSO, lapatinib (0.5 μmol/L), PP2 (2 μmol/L) alone, or in combination. The data is shown as fold change in viability relative to DMSO control and is representative of three independent experiments (means ± SEM). *, P < 0.05; ***, P < 0.001. Jacqueline R. Ha et al. Mol Cancer Res 2018;16:894-908 ©2018 by American Association for Cancer Research