Receptor Tyrosine Kinases: Role in Cancer Progression

Retraction of ‘Linc00472 suppresses breast cancer progression and enhances doxorubicin sensitivity through regulation of miR-141 and programmed cell death 4’ by Pengwei Lu et al., RSC Adv., 2018, 8, 8455–8468, DOI: 10.1039/C8RA00296G

Download Full-text

Suppression of cell proliferation and programmed cell death by dexamethasone during postnatal lung development

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00406.2000 ◽

2002 ◽

Vol 282 (3) ◽

pp. L477-L483 ◽

Cited By ~ 31

Author(s):

Cédric Luyet ◽

Peter H. Burri ◽

Johannes C. Schittny

Keyword(s):

Cell Proliferation ◽

Cell Death ◽

Programmed Cell Death ◽

Lung Development ◽

Structural Changes ◽

Tissue Transglutaminase ◽

Lung Parenchyma ◽

Lung Maturation ◽

Morphological Criteria ◽

Postnatal Lung Development

Prematurely born babies are often treated with glucocorticoids. We studied the consequences of an early postnatal and short dexamethasone treatment (0.1–0.01 μg/g, days 1–4) on lung development in rats, focusing on its influence on peaks of cell proliferation around day 4 and of programmed cell death at days 19–21. By morphological criteria, we observed a dexamethasone-induced premature maturation of the septa ( day 4), followed by a transient septal immatureness and delayed alveolarization leading to complete rescue of the structural changes. The numbers of proliferating (anti-Ki67) and dying cells (TdT-mediated dUTP nick end labeling) were determined and compared with controls. In dexamethasone-treated animals, both the peak of cell proliferation and the peak of programmed cell death were reduced to baseline, whereas the expression of tissue transglutaminase (transglutaminase-C), another marker for postnatal lung maturation, was not significantly altered. We hypothesize that a short neonatal course of dexamethasone leads to severe but transient structural changes of the lung parenchyma and influences the balance between cell proliferation and cell death even in later stages of lung maturation.

Download Full-text

miR-103 Functions as a Tumor Suppressor by Directly Targeting Programmed Cell Death 10 in NSCLC

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics ◽

10.3727/096504017x15000757094686 ◽

2018 ◽

Vol 26 (4) ◽

pp. 519-528 ◽

Cited By ~ 10

Author(s):

Dong Yang ◽

Jian-Jun Wang ◽

Jin-Song Li ◽

Qian-Yu Xu

Keyword(s):

Lung Cancer ◽

Cell Proliferation ◽

Cell Death ◽

Programmed Cell Death ◽

Tumor Size ◽

Apoptotic Cell ◽

A549 Cells ◽

Invasion And Migration ◽

Metastatic Capacity ◽

And Migration

Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. Absence of miR-103 has recently been identified to be associated with metastatic capacity of primary lung tumors. However, the exact role of miR-103 in NSCLC and the molecular mechanism are unclear. In the present study, we showed that miR-103 expression was reduced in NSCLC tissues and cells. miR-103 expression was negatively correlated with tumor size and stage. The overall survival was longer in patients with higher miR-103 level than in those with lower miR-103 expression. miR-103 inhibited cell proliferation in A549 cells, decreased tumor weight and volume, and prolonged survival of tumor-implanted nude mice. miR-103 increased apoptotic cell death in A549 cells. Furthermore, miR-103 decreased the invasion and migration abilities in A549 cells, as evidenced by Transwell and wound healing results. Downregulation of miR-103 significantly reduced the level of programmed cell death 10 (PDCD10). We found a significant decrease in the relative luciferase activity of the reporter gene in A549 cells cotransfected with the miR-103 mimic and pGL3-PDCD10 WT 3′-UTR, but not pGL3-PDCD10 mut 3′-UTR. We showed that overexpression of PDCD10 significantly inhibited miR-103-induced inhibition of cell proliferation, increased apoptosis, and decreased invasion and migration in A549 cells. Moreover, we found that PDCD10 expression was increased in NSCLC tissues and cells. PDCD10 expression was positively correlated with tumor size and stage. Overexpression of PDCD10 increased cell proliferation and inhibited apoptosis in A549 cells. The data demonstrated that dysregulation of the miR-103/PDCD10 signal may be a novel therapeutic target for the treatment of NSCLC.

Download Full-text

Evaluating the Remote Control of Programmed Cell Death, with or without a Compensatory Cell Proliferation

International Journal of Biological Sciences ◽

10.7150/ijbs.26962 ◽

2018 ◽

Vol 14 (13) ◽

pp. 1800-1812 ◽

Cited By ~ 1

Author(s):

Xixi Dou ◽

Lichan Chen ◽

Mingjuan Lei ◽

Lucas Zellmer ◽

Qingwen Jia ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Death ◽

Remote Control ◽

Programmed Cell Death

Download Full-text

Two-Pulse Endosomal Stimulation of Receptor Tyrosine Kinases Induces Cell Proliferation

Methods in Molecular Biology - ErbB Receptor Signaling ◽

10.1007/978-1-4939-7219-7_9 ◽

2017 ◽

pp. 127-133

Author(s):

Steven Pennock ◽

Sukhmani Billing ◽

Zhixiang Wang ◽

Yi Wang

Keyword(s):

Cell Proliferation ◽

Tyrosine Kinases ◽

Receptor Tyrosine Kinases ◽

Stimulation Of

Download Full-text

The Importance of Exosomal PD-L1 in Cancer Progression and Its Potential as a Therapeutic Target

Cells ◽

10.3390/cells10113247 ◽

2021 ◽

Vol 10 (11) ◽

pp. 3247

Author(s):

Lingxiao Ye ◽

Zhengxin Zhu ◽

Xiaochuan Chen ◽

Haoran Zhang ◽

Jiaqi Huang ◽

...

Keyword(s):

Drug Resistance ◽

Cell Death ◽

Programmed Cell Death ◽

Cancer Progression ◽

T Cell Activation ◽

Cell Activation ◽

Immune Escape ◽

Tumor Treatment

Binding of programmed cell death ligand 1 (PD-L1) to its receptor programmed cell death protein 1 (PD-1) can lead to the inactivation of cytotoxic T lymphocytes, which is one of the mechanisms for immune escape of tumors. Immunotherapy based on this mechanism has been applied in clinic with some remaining issues such as drug resistance. Exosomal PD-L1 derived from tumor cells is considered to play a key role in mediating drug resistance. Here, the effects of various tumor-derived exosomes and tumor-derived exosomal PD-L1 on tumor progression are summarized and discussed. Researchers have found that high expression of exosomal PD-L1 can inhibit T cell activation in in vitro experiments, but the function of exosomal PD-L1 in vivo remains controversial. In addition, the circulating exosomal PD-L1 has high potential to act as an indicator to evaluate the clinical effect. Moreover, therapeutic strategy targeting exosomal PD-L1 is discussed, such as inhibiting the biogenesis or secretion of exosomes. Besides, some specific methods based on the strategy of inhibiting exosomes are concluded. Further study of exosomal PD-L1 may provide an effective and safe approach for tumor treatment, and targeting exosomal PD-L1 by inhibiting exosomes may be a potential method for tumor treatment.

Download Full-text

Receptor Tyrosine Kinases and Their Signaling Pathways as Therapeutic Targets of Curcumin in Cancer

Frontiers in Pharmacology ◽

10.3389/fphar.2021.772510 ◽

2021 ◽

Vol 12 ◽

Author(s):

Sareshma Sudhesh Dev ◽

Syafiq Asnawi Zainal Abidin ◽

Reyhaneh Farghadani ◽

Iekhsan Othman ◽

Rakesh Naidu

Keyword(s):

Signaling Pathways ◽

Cancer Progression ◽

Tyrosine Kinases ◽

Receptor Tyrosine Kinases ◽

Surface Proteins ◽

Downstream Signaling ◽

Anti Cancer ◽

Rtk Inhibitors

Receptor tyrosine kinases (RTKs) are transmembrane cell-surface proteins that act as signal transducers. They regulate essential cellular processes like proliferation, apoptosis, differentiation and metabolism. RTK alteration occurs in a broad spectrum of cancers, emphasising its crucial role in cancer progression and as a suitable therapeutic target. The use of small molecule RTK inhibitors however, has been crippled by the emergence of resistance, highlighting the need for a pleiotropic anti-cancer agent that can replace or be used in combination with existing pharmacological agents to enhance treatment efficacy. Curcumin is an attractive therapeutic agent mainly due to its potent anti-cancer effects, extensive range of targets and minimal toxicity. Out of the numerous documented targets of curcumin, RTKs appear to be one of the main nodes of curcumin-mediated inhibition. Many studies have found that curcumin influences RTK activation and their downstream signaling pathways resulting in increased apoptosis, decreased proliferation and decreased migration in cancer both in vitro and in vivo. This review focused on how curcumin exhibits anti-cancer effects through inhibition of RTKs and downstream signaling pathways like the MAPK, PI3K/Akt, JAK/STAT, and NF-κB pathways. Combination studies of curcumin and RTK inhibitors were also analysed with emphasis on their common molecular targets.

Download Full-text