Persistent pain accelerates xenograft tumor growth of breast cancer in rat

2018 ◽  
Vol 495 (4) ◽  
pp. 2432-2438 ◽  
Author(s):  
Jing Li ◽  
Yunheng Sun ◽  
Gang Ding ◽  
Feng Jiang
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Persistent Pain ◽  
Xenograft Tumor ◽  
Xenograft Tumor Growth

scholarly journals Evaluation of the pharmacological activities of RAD1901, a selective estrogen receptor degrader

2015 ◽  
Vol 22 (5) ◽  
pp. 713-724 ◽  
Author(s):  
Suzanne E Wardell ◽  
Erik R Nelson ◽  
Christina A Chao ◽  
Holly M Alley ◽  
Donald P McDonnell
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Tumor Growth ◽  
Endocrine Therapy ◽  
Cancer Metastasis ◽  
Xenograft Tumor ◽  
Metastatic Setting ◽  
Dose Dependent ◽  
The Brain ◽  
Xenograft Tumor Growth

Endocrine therapy, using tamoxifen or an aromatase inhibitor, remains a first-line treatment for estrogen receptor 1 (ESR1) positive breast cancer. However, tumor resistance limits the duration of response. The clinical efficacy of fulvestrant, a selective ER degrader (SERD) that triggers receptor degradation, has confirmed that ESR1 often remains engaged in endocrine therapy resistant cancers. Recently developed, selective ER modulators (SERMs)/SERD hybrids (SSHs) that facilitate ESR1 degradation in breast cancer cells and reproductive tissues have been advanced as an alternative treatment for advanced breast cancer, particularly in the metastatic setting. RAD1901 is one SSH currently being evaluated clinically that is unique among ESR1 modulators in that it readily enters the brain, a common site of breast cancer metastasis. In this study, RAD1901 inhibited estrogen activation of ESR1in vitroandin vivo, inhibited estrogen-dependent breast cancer cell proliferation and xenograft tumor growth, and mediated dose-dependent downregulation of ESR1 protein. However, doses of RAD1901 insufficient to induce ESR1 degradation were shown to result in the activation of ESR1 target genes and in the stimulation of xenograft tumor growth. RAD1901 is an SSH that exhibits complex pharmacology in breast cancer models, having dose-dependent agonist/antagonist activity displayed in a tissue-selective manner. It remains unclear how this unique pharmacology will impact the utility of RAD1901 for breast cancer treatment. However, being the only SERD currently known to access the brain, RAD1901 merits evaluation as a targeted therapy for the treatment of breast cancer brain metastases.

Circ_002059 suppresses cell proliferation and migration of gastric cancer via miR-182/MTSS1 axis

2021 ◽  
Vol 53 (4) ◽  
pp. 454-462
Author(s):  
Ting Li ◽  
Xiaomin Zuo ◽  
Xiangling Meng
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Luciferase Reporter ◽  
Metastasis Suppressor ◽  
Xenograft Tumor ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Xenograft Tumor Growth ◽  
Proliferation And Migration

Abstract Circular RNAs (circRNAs) play either oncogenic or tumor suppressive roles in gastric cancer (GC). A previous study demonstrated that circ_002059, a typical circRNA, was downregulated in GC tissues. However, the role and mechanism of circ_002059 in GC development are still unknown. In this study, the levels of circ_002059, miR-182, and metastasis suppressor-1 (MTSS1) were examined by real-time quantitative polymerase chain reaction and western blot analysis. Cell proliferation and migration were evaluated by MTT assay and Transwell migration assay, respectively. The interactions between miR-182 and circ_002059 or MTSS1 were analyzed by dual-luciferase reporter assay. A GC xenograft model was established to validate the role of circ_002059 in GC progression in vivo. Overexpression of circ_002059 significantly inhibited, whereas knockdown of circ_002059 notably facilitated, cell proliferation and migration in GC cells. MTSS1 was found to be a direct target of miR-182 and circ_002059 upregulated MTSS1 expression by competitively sponging miR-182. Transfection with miR-182 mimic and MTSS1 silencing abated the inhibitory effect of circ_002059 on GC progression. Circ_002059 inhibited GC cell xenograft tumor growth by regulating miR-182 and MTSS1 expression. Collectively, Circ_002059 inhibited GC cell proliferation and migration in vitro and xenograft tumor growth in mice, by regulating the miR-182/MTSS1 axis.

scholarly journals  -Mangostin, a xanthone from mangosteen fruit, promotes cell cycle arrest in prostate cancer and decreases xenograft tumor growth

2011 ◽  
Vol 33 (2) ◽  
pp. 413-419 ◽  
Author(s):  
J. J. Johnson ◽  
S. M. Petiwala ◽  
D. N. Syed ◽  
J. T. Rasmussen ◽  
V. M. Adhami ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Tumor Growth ◽  
Cell Cycle Arrest ◽  
Xenograft Tumor ◽  
Cycle Arrest ◽  
Xenograft Tumor Growth

scholarly journals Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Tongue Squamous Cell Carcinoma

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Yi Liu ◽  
Rong-Hua Li ◽  
Gang Ren ◽  
Jin Jiang
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Protein Expression ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Oral Carcinoma ◽  
Xenograft Tumor ◽  
Protein Expression Level ◽  
Xenograft Tumor Growth

Background. Oral carcinoma is the sixth most common cancer and is a serious public health problem, and tongue squamous cell carcinoma (TSCC) is the most common type of oral carcinoma. Kinesin family member 22 (KIF22), also called as kinesin-like DNA binding protein (KID), is a microtubule-based motor protein and binds to both microtubules and chromosomes, transporting organelles, protein, and mRNA. This research aimed at investigating the prognostic significance of KIF22 in TSCC. Patients and Methods. This retrospective research collected 82 paired tissues with TSCC. KIF22 protein expression level was detected by immunohistochemical staining. Suppression of KIF22 with shRNA in CAL-27 and SCC-15 cells was to observe cell proliferation in vitro and xenograft tumor growth in vivo. Results. In TSCC tissues, the protein expression level of KIF22 was increased and correlated with tumor stage, clinical stage, and lymphatic metastasis (P=0.013, P=0.034 and P=0.015, respectively). Suppression of KIF22 inhibited cell proliferation and xenograft tumor growth. Conclusion. KIF22 might play an important role in the progression of TSCC and could serve as a therapeutic target for TSCC.

scholarly journals Novel synthetic bisindolylmaleimide alkaloids inhibit STAT3 activation by binding to the SH2 domain and suppress breast xenograft tumor growth

Oncogene ◽  
2018 ◽  
Vol 37 (18) ◽  
pp. 2469-2480 ◽  
Author(s):  
Xia Li ◽  
Hongguang Ma ◽  
Lin Li ◽  
Yifan Chen ◽  
Xiao Sun ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Sh2 Domain ◽  
Xenograft Tumor ◽  
Xenograft Tumor Growth
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