Cancer-associated fibroblasts (CAFs) in thyroid papillary carcinoma: molecular networks and interactions

2021 ◽  
pp. jclinpath-2020-207357
Author(s):  
Jeehoon Ham ◽  
Bin Wang ◽  
Joseph William Po ◽  
Amandeep Singh ◽  
Navin Niles ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Stromal Cells ◽  
Cancer Metastasis ◽  
Current Knowledge ◽  
Molecular Networks ◽  
Cancer Cell Growth ◽  
Molecular Events

In 1989, Stephen Paget proposed the ‘seed and soil’ theory of cancer metastasis. This theory has led to previous researchers focusing on the role of a tumour as a cancer seed and antiangiogenesis agents as cancer soil fumigant; for the latter to be effective, it is important for them to be able to distinguish cancer cells from stromal cells. However, antiangiogenesis agents have not produced dramatic survival benefits in vivo. This may be related to their inability to destroy the supporting stroma that promote cancer cell growth. Therefore, in order to effectively arrest cancer cell growth for therapeutic purposes, a paradigm shift is required in our fundamental approach to decipher the molecular events and networks in the stromal environment that cancer cells can thrive and proliferate. The pathogenesis of cancer is a multidimensional process of pathological molecular and cellular pathways, influencing different stromal properties and achieving a mutually negotiated crosstalk between cancer cells and stromal cells. This review summarises the clinical presentation of current knowledge of classical papillary thyroid carcinoma (PTC), emerging molecular diagnostics and future directions of classical PTC research.

scholarly journals Mitochondrial supercomplex assembly promotes breast and endometrial tumorigenesis by metabolic alterations and enhanced hypoxia tolerance

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Kazuhiro Ikeda ◽  
Kuniko Horie-Inoue ◽  
Takashi Suzuki ◽  
Rutsuko Hobo ◽  
Norie Nakasato ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Tricarboxylic Acid Cycle ◽  
Hypoxia Tolerance ◽  
Breast Cancer Patients ◽  
Cancer Cell Growth

Abstract Recent advance in cancer research sheds light on the contribution of mitochondrial respiration in tumorigenesis, as they efficiently produce ATP and oncogenic metabolites that will facilitate cancer cell growth. Here we show that a stabilizing factor for mitochondrial supercomplex assembly, COX7RP/COX7A2L/SCAF1, is abundantly expressed in clinical breast and endometrial cancers. Moreover, COX7RP overexpression associates with prognosis of breast cancer patients. We demonstrate that COX7RP overexpression in breast and endometrial cancer cells promotes in vitro and in vivo growth, stabilizes mitochondrial supercomplex assembly even in hypoxic states, and increases hypoxia tolerance. Metabolomic analyses reveal that COX7RP overexpression modulates the metabolic profile of cancer cells, particularly the steady-state levels of tricarboxylic acid cycle intermediates. Notably, silencing of each subunit of the 2-oxoglutarate dehydrogenase complex decreases the COX7RP-stimulated cancer cell growth. Our results indicate that COX7RP is a growth-regulatory factor for breast and endometrial cancer cells by regulating metabolic pathways and energy production.

scholarly journals Levobupivacaine Induces Ferroptosis by miR-489-3p/SLC7A11 Signaling in Gastric Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Shun-Hong Mao ◽  
Chun-Hua Zhu ◽  
Yu Nie ◽  
Jian Yu ◽  
Lei Wang
Keyword(s):  
Gastric Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Local Anesthetic ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Cancer Cell Growth

Gastric cancer is one of the most the prevalent malignancies and the therapeutic strategies for patients with gastric cancer remains limited. Local anesthetic levobupivacaine has demonstrated potential anti-cancer property, but its correlation with gastric cancer and ferroptosis is poor understood. Here, we identified the novel function of levobupivacaine in regulating ferroptosis of gastric cancer cells. The treatment of levobupivacaine suppressed gastric cancer cell viabilities and Edu-positive cell proportions. The gastric cancer cell growth was reduced by levobupivacaine in vivo. Moreover, the treatment of levobupivacaine enhanced erastin-induced inhibitory impact on gastric cancer cell viabilities. The levels of Fe2+/iron and lipid ROS were induced by levobupivacaine in erastin and RSL3-stimulated gastric cancer cells. levobupivacaine-upregulated miR-489-3p enhanced ferroptosis of gastric cancer cells by targeting SLC7A11. MiR-489-3p was involved in levobupivacaine-induced ferroptosis of gastric cancer cells. Levobupivacaine/miR-489-3p/SLC7A11 axis attenuates gastric cancer cell proliferation in vitro. Therefore, we concluded that the local anesthetic levobupivacaine induced ferroptosis of gastric cancer cells to repress gastric cancer cell growth by miR-489-3p/SLC7A11 axis.

794: Valproic Acid Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo

2006 ◽  
Vol 175 (4S) ◽  
pp. 257-257
Author(s):  
Jennifer Sung ◽  
Qinghua Xia ◽  
Wasim Chowdhury ◽  
Shabana Shabbeer ◽  
Michael Carducci ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Valproic Acid ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Growth

scholarly journals HOXB4 inhibits the proliferation and tumorigenesis of cervical cancer cells by downregulating the activity of Wnt/β-catenin signaling pathway

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Dan Lei ◽  
Wen-Ting Yang ◽  
Peng-Sheng Zheng
Keyword(s):  
Cervical Cancer ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Tumor Formation ◽  
Cervical Cancer Cell ◽  
Cancer Cell Growth ◽  
Bioinformatics Analyses

AbstractHomeobox B4 (HOXB4), which belongs to the homeobox (HOX) family, possesses transcription factor activity and has a crucial role in stem cell self-renewal and tumorigenesis. However, its biological function and exact mechanism in cervical cancer remain unknown. Here, we found that HOXB4 was markedly downregulated in cervical cancer. We demonstrated that HOXB4 obviously suppressed cervical cancer cell proliferation and tumorigenic potential in nude mice. Additionally, HOXB4-induced cell cycle arrest at the transition from the G0/G1 phase to the S phase. Conversely, loss of HOXB4 promoted cervical cancer cell growth both in vitro and in vivo. Bioinformatics analyses and mechanistic studies revealed that HOXB4 inhibited the activity of the Wnt/β-catenin signaling pathway by direct transcriptional repression of β-catenin. Furthermore, β-catenin re-expression rescued HOXB4-induced cervical cancer cell defects. Taken together, these findings suggested that HOXB4 directly transcriptional repressed β-catenin and subsequently inactivated the Wnt/β-catenin signaling pathway, leading to significant inhibition of cervical cancer cell growth and tumor formation.

scholarly journals Deferasirox, an oral iron chelator, with gemcitabine synergistically inhibits pancreatic cancer cell growth in vitro and in vivo

Oncotarget ◽  
2018 ◽  
Vol 9 (47) ◽  
pp. 28434-28444 ◽  
Author(s):  
Shuhei Shinoda ◽  
Seiji Kaino ◽  
Shogo Amano ◽  
Hirofumi Harima ◽  
Toshihiko Matsumoto ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Iron Chelator ◽  
Oral Iron ◽  
Cancer Cell Growth ◽  
Oral Iron Chelator

Fibrin and Cancer Cell Growth: Problems in the Evaluation of Experimental Models

1979 ◽  
Author(s):  
Andreina Poggi
Keyword(s):  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Primary Tumour ◽  
Antiplatelet Agent ◽  
Experimental Models ◽  
Surgical Removal ◽  
Antiinflammatory Drugs ◽  
Cancer Cell Growth ◽  
Lung Carcinoma Cells

Studies on the role of fibrin in experimental cancer growth should take into account the following problems: 1) during growth and dissemination of experimental tumours, haemostatic changes may occur which vary depending on the route of inoculation of cancer cells and on the tissue wherethe tumour grows. Thrombocytopenia, haemolytic microangiopathic anaemia and decreased survival of fibrinogen were observed during spontaneous dissemination to the lung of i.m. implanted Lewis Lung Carcinoma cells, not when metastatic growth occurred after surgical removal of the primary tumour or lung nodules developed following i.v. injection of the same cells. 2) Treatment of experimental tumours with drugs active on the haemostatic system may have different effects depending on the stage of growth of the tumour. This observation (which we have made with both warfarin and a defibrinating enzyme in murine metastasizing tumours) could suggest that fibrin may play different roles at different phases of cancer cell growth. 3) The supposed antiturooral activity of drugs active on the haemostatic system may be also influenced by other factors, such as a direct activity on cancer cells or on the host’s immune system or on blood supply to the tumour. As an example, non steroidal antiinflammatory drugs may act not only as antiplatelet agent but also as inhibitors of prostaglandin synthesis by cancer cells and some snake venoms may influence cancer cell growth not only through defibrination, but also with their iinnu-nodepressant properties. (Supported by Italian CNR and NIM. MCI, USA).

Cordycepin inhibits pancreatic cancer cell growth in vitro and in vivo via targeting FGFR2 and blocking ERK signaling

2020 ◽  
Vol 18 (5) ◽  
pp. 345-355
Author(s):  
Xue-Ying LI ◽  
Homng TAO ◽  
Can JIN ◽  
Zhen-Yun DU ◽  
Wen-Feng LIAO ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Erk Signaling ◽  
Cancer Cell Growth
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