Special Issue "Cancer Cell Proliferation"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (31 March 2015)

Special Issue Editor

Guest Editor
Dr. Vita Golubovskaya

1. Research and Business Development, Promab Biotechnologies, 2600 Hilltop Drive, Richmond, CA 94806, USA
2. Department of Medicine, University of Oklahoma, Oklahoma City, OK 73126, USA
Website | E-Mail
Interests: Immunotherapy; CAR-T cells; tumor microenvironment; checkpoint protein; hypoxia; tumor survival signaling

Special Issue Information

Dear Colleagues,

Cancer cell growth and proliferation can be activated by extracellular growth factors that bind to tyrosine kinase receptors or by extracellular matrix-integrin-focal adhesion kinase, Src signaling and its down-stream signaling pathways. In many cancer types, abnormal regulation of tyrosine kinase receptor signaling (TKR)s plays a role in cell cycle, proliferation, survival and oncogenesis. Targeting cancer cell proliferation by inhibiting TKRs, integrins and its down-stream intracellular signaling pathways is a potential approach to development of anticancer targeted therapy.

Dr. Vita Golubovskaya
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • growth factor receptors
  • proliferation
  • apoptosis
  • survival
  • angiogenesis
  • integrin
  • tyrosine kinase
  • intracellular survival signaling
  • focal adhesion kinase
  • src

Published Papers (9 papers)

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Research

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Open AccessArticle Hypermethylation of MAPK13 Promoter in Oesophageal Squamous Cell Carcinoma Is Associated with Loss of p38δ MAPK Expression
Cancers 2015, 7(4), 2124-2133; https://doi.org/10.3390/cancers7040881
Received: 2 July 2015 / Revised: 14 October 2015 / Accepted: 15 October 2015 / Published: 23 October 2015
Cited by 1 | PDF Full-text (1223 KB) | HTML Full-text | XML Full-text
Abstract
The loss of tumour suppressor gene function is a hallmark of malignant transformation and can occur by a variety of genetic and/or epigenetic alterations. We have previously characterised p38δ mitogen-activated protein kinase (MAPK) as a tumour suppressor in oesophageal squamous cell carcinoma (OESCC) [...] Read more.
The loss of tumour suppressor gene function is a hallmark of malignant transformation and can occur by a variety of genetic and/or epigenetic alterations. We have previously characterised p38δ mitogen-activated protein kinase (MAPK) as a tumour suppressor in oesophageal squamous cell carcinoma (OESCC) and outlined how loss of p38δ MAPK expression promotes increased proliferation and migration, as well as reduced chemosensitivity. Our aim was to investigate the underlying molecular causes of loss of p38δ MAPK expression in OESCC. Sequence analysis of DNA from p38δ MAPK positive and p38δ MAPK negative OESCC cell lines was used to investigate potential loss of function causing mutations. Epigenetic control of p38δ expression in OESCC was examined using methylation-specific PCR and sequencing of bisulfite-converted DNA. We did not identify any mutations in the MAPK13 sequence in OESCC cell lines which lack p38δ MAPK expression. However, we identified a differential pattern of methylation between p38δ MAPK positive and p38δ MAPK negative cell lines. We outline here for the first time differential MAPK13 promoter methylation in OESCC. Our results suggest that epigenetic alterations are responsible, in part, for the suppression of p38δ MAPK expression and promotion of tumourigenesis in OESCC. Full article
(This article belongs to the Special Issue Cancer Cell Proliferation)
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Open AccessArticle Silencing of Taxol-Sensitizer Genes in Cancer Cells: Lack of Sensitization Effects
Cancers 2015, 7(2), 1052-1071; https://doi.org/10.3390/cancers7020824
Received: 1 April 2015 / Accepted: 3 June 2015 / Published: 16 June 2015
Cited by 3 | PDF Full-text (2248 KB) | HTML Full-text | XML Full-text
Abstract
A previous genome-wide screening analysis identified a panel of genes that sensitize the human non-small-cell lung carcinoma cell line NCI-H1155 to taxol. However, whether the identified genes sensitize other cancer cells to taxol has not been examined. Here, we silenced the taxol-sensitizer genes [...] Read more.
A previous genome-wide screening analysis identified a panel of genes that sensitize the human non-small-cell lung carcinoma cell line NCI-H1155 to taxol. However, whether the identified genes sensitize other cancer cells to taxol has not been examined. Here, we silenced the taxol-sensitizer genes identified (acrbp, atp6v0d2, fgd4, hs6st2, psma6, and tubgcp2) in nine other cancer cell types (including lung, cervical, ovarian, and hepatocellular carcinoma cell lines) that showed reduced cell viability in the presence of a sub-lethal concentration of taxol. Surprisingly, none of the genes studied increased sensitivity to taxol in the tested panel of cell lines. As observed in H1155 cells, SKOV3 cells displayed induction of five of the six genes studied in response to a cell killing dose of taxol. The other cell types were much less responsive to taxol. Notably, four of the five inducible taxol-sensitizer genes tested (acrbp, atp6v0d2, psma6, and tubgcp2) were upregulated in a taxol-resistant ovarian cancer cell line. These results indicate that the previously identified taxol-sensitizer loci are not conserved genetic targets involved in inhibiting cell proliferation in response to taxol. Our findings also suggest that regulation of taxol-sensitizer genes by taxol may be critical for acquired cell resistance to the drug. Full article
(This article belongs to the Special Issue Cancer Cell Proliferation)
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Review

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Open AccessReview Cell Proliferation in Neuroblastoma
Received: 20 November 2015 / Revised: 5 January 2016 / Accepted: 8 January 2016 / Published: 12 January 2016
Cited by 7 | PDF Full-text (286 KB) | HTML Full-text | XML Full-text
Abstract
Neuroblastoma, the most common extracranial solid tumor of childhood, continues to carry a dismal prognosis for children diagnosed with advanced stage or relapsed disease. This review focuses upon factors responsible for cell proliferation in neuroblastoma including transcription factors, kinases, and regulators of the [...] Read more.
Neuroblastoma, the most common extracranial solid tumor of childhood, continues to carry a dismal prognosis for children diagnosed with advanced stage or relapsed disease. This review focuses upon factors responsible for cell proliferation in neuroblastoma including transcription factors, kinases, and regulators of the cell cycle. Novel therapeutic strategies directed toward these targets in neuroblastoma are discussed. Full article
(This article belongs to the Special Issue Cancer Cell Proliferation)
Open AccessReview Roles of TRPM8 Ion Channels in Cancer: Proliferation, Survival, and Invasion
Cancers 2015, 7(4), 2134-2146; https://doi.org/10.3390/cancers7040882
Received: 13 June 2015 / Revised: 15 October 2015 / Accepted: 15 October 2015 / Published: 23 October 2015
Cited by 19 | PDF Full-text (599 KB) | HTML Full-text | XML Full-text
Abstract
The goal of this article is to provide a critical review of the transient receptor potential melastatin-subfamily member 8 (TRPM8) in cancers, with an emphasis on its roles in cellular proliferation, survival, and invasion. The TRPM8 ion channels regulate Ca²⁺ homeostasis and function [...] Read more.
The goal of this article is to provide a critical review of the transient receptor potential melastatin-subfamily member 8 (TRPM8) in cancers, with an emphasis on its roles in cellular proliferation, survival, and invasion. The TRPM8 ion channels regulate Ca²⁺ homeostasis and function as a cellular sensor and transducer of cold temperature. Accumulating evidence has demonstrated that TRPM8 is aberrantly expressed in a variety of malignant solid tumors. Clinicopathological analysis has shown that over-expression of TRPM8 correlates with tumor progression. Experimental data have revealed important roles of TRPM8 channels in cancer cells proliferation, survival, and invasion, which appear to be dependent on the cancer type. Recent reports have begun to reveal the signaling mechanisms that mediate the biological roles of TRPM8 in tumor growth and metastasis. Determining the mechanistic roles of TRPM8 in cancer is expected to elucidate the impact of thermal and chemical stimuli on the formation and progression of neoplasms. Translational research and clinical investigation of TRPM8 in malignant diseases will help exploit these ion channels as molecular biomarkers and therapeutic targets for developing precision cancer medicine. Full article
(This article belongs to the Special Issue Cancer Cell Proliferation)
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Open AccessReview Targeting RTK Signaling Pathways in Cancer
Cancers 2015, 7(3), 1758-1784; https://doi.org/10.3390/cancers7030860
Received: 4 May 2015 / Revised: 24 August 2015 / Accepted: 26 August 2015 / Published: 3 September 2015
Cited by 67 | PDF Full-text (821 KB) | HTML Full-text | XML Full-text
Abstract
The RAS/MAP kinase and the RAS/PI3K/AKT pathways play a key role in the regulation of proliferation, differentiation and survival. The induction of these pathways depends on Receptor Tyrosine Kinases (RTKs) that are activated upon ligand binding. In cancer, constitutive and aberrant activations of [...] Read more.
The RAS/MAP kinase and the RAS/PI3K/AKT pathways play a key role in the regulation of proliferation, differentiation and survival. The induction of these pathways depends on Receptor Tyrosine Kinases (RTKs) that are activated upon ligand binding. In cancer, constitutive and aberrant activations of components of those pathways result in increased proliferation, survival and metastasis. For instance, mutations affecting RTKs, Ras, B-Raf, PI3K and AKT are common in perpetuating the malignancy of several types of cancers and from different tissue origins. Therefore, these signaling pathways became prime targets for cancer therapy. This review aims to provide an overview about the most frequently encountered mutations, the pathogenesis that results from such mutations and the known therapeutic strategies developed to counteract their aberrant functions. Full article
(This article belongs to the Special Issue Cancer Cell Proliferation)
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Open AccessReview Dichotomy in the Epigenetic Mark Lysine Acetylation is Critical for the Proliferation of Prostate Cancer Cells
Cancers 2015, 7(3), 1622-1642; https://doi.org/10.3390/cancers7030854
Received: 25 June 2015 / Revised: 7 August 2015 / Accepted: 11 August 2015 / Published: 19 August 2015
Cited by 1 | PDF Full-text (1436 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
The dynamics of lysine acetylation serve as a major epigenetic mark, which regulates cellular response to inflammation, DNA damage and hormonal changes. Microarray assays reveal changes in gene expression, but cannot predict regulation of a protein function by epigenetic modifications. The present study [...] Read more.
The dynamics of lysine acetylation serve as a major epigenetic mark, which regulates cellular response to inflammation, DNA damage and hormonal changes. Microarray assays reveal changes in gene expression, but cannot predict regulation of a protein function by epigenetic modifications. The present study employs computational tools to inclusively analyze microarray data to understand the potential role of acetylation during development of androgen-independent PCa. The data revealed that the androgen receptor interacts with 333 proteins, out of which at least 92 proteins were acetylated. Notably, the number of cellular proteins undergoing acetylation in the androgen-dependent PCa was more as compared to the androgen-independent PCa. Specifically, the 32 lysine-acetylated proteins in the cellular models of androgen-dependent PCa were mainly involved in regulating stability as well as pre- and post-processing of mRNA. Collectively, the data demonstrate that protein lysine acetylation plays a crucial role during the transition of androgen-dependent to -independent PCa, which importantly, could also serve as a functional axis to unravel new therapeutic targets. Full article
(This article belongs to the Special Issue Cancer Cell Proliferation)
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Open AccessReview Targeting Protein Kinase C Downstream of Growth Factor and Adhesion Signalling
Cancers 2015, 7(3), 1271-1291; https://doi.org/10.3390/cancers7030836
Received: 27 March 2015 / Revised: 25 May 2015 / Accepted: 3 July 2015 / Published: 15 July 2015
Cited by 8 | PDF Full-text (894 KB) | HTML Full-text | XML Full-text
Abstract
The signaling outputs of Receptor Tyrosine Kinases, G-protein coupled receptors and integrins converge to mediate key cell process such as cell adhesion, cell migration, cell invasion and cell proliferation. Once activated by their ligands, these cell surface proteins recruit and direct a diverse [...] Read more.
The signaling outputs of Receptor Tyrosine Kinases, G-protein coupled receptors and integrins converge to mediate key cell process such as cell adhesion, cell migration, cell invasion and cell proliferation. Once activated by their ligands, these cell surface proteins recruit and direct a diverse range of proteins to disseminate the appropriate response downstream of the specific environmental cues. One of the key groups of proteins required to regulate these activities is the family of serine/threonine intracellular kinases called Protein Kinase Cs. The activity and subcellular location of PKCs are mediated by a series of tightly regulated events and is dependent on several posttranslational modifications and the availability of second messengers. Protein Kinase Cs exhibit both pro- and anti-tumorigenic effects making them an interesting target for anti-cancer treatment. Full article
(This article belongs to the Special Issue Cancer Cell Proliferation)
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Open AccessReview Involvement of 14-3-3 Proteins in Regulating Tumor Progression of Hepatocellular Carcinoma
Cancers 2015, 7(2), 1022-1036; https://doi.org/10.3390/cancers7020822
Received: 4 May 2015 / Accepted: 10 June 2015 / Published: 15 June 2015
Cited by 20 | PDF Full-text (277 KB) | HTML Full-text | XML Full-text
Abstract
There are seven mammalian isoforms of the 14-3-3 protein, which regulate multiple cellular functions via interactions with phosphorylated partners. Increased expression of 14-3-3 proteins contributes to tumor progression of various malignancies. Several isoforms of 14-3-3 are overexpressed and associate with higher metastatic risks [...] Read more.
There are seven mammalian isoforms of the 14-3-3 protein, which regulate multiple cellular functions via interactions with phosphorylated partners. Increased expression of 14-3-3 proteins contributes to tumor progression of various malignancies. Several isoforms of 14-3-3 are overexpressed and associate with higher metastatic risks and poorer survival rates of hepatocellular carcinoma (HCC). 14-3-3β and 14-3-3ζ regulate HCC cell proliferation, tumor growth and chemosensitivity via modulating mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK) and p38 signal pathways. Moreover, 14-3-3ε suppresses E-cadherin and induces focal adhesion kinase (FAK) expression, thereby enhancing epithelial-mesenchymal transition (EMT) and HCC cell migration. 14-3-3ζ forms complexes with αB-crystallin, which induces EMT and is the cause of sorafenib resistance in HCC. Finally, a recent study has indicated that 14-3-3σ induces heat shock protein 70 (HSP70) expression, which increases HCC cell migration. These results suggest that selective 14-3-3 isoforms contribute to cell proliferation, EMT and cell migration of HCC by regulating distinct targets and signal pathways. Targeting 14-3-3 proteins together with specific downstream effectors therefore has potential to be therapeutic and prognostic factors of HCC. In this article, we will overview 14-3-3's regulation of its downstream factors and contributions to HCC EMT, cell migration and proliferation. Full article
(This article belongs to the Special Issue Cancer Cell Proliferation)
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Open AccessReview Voltage-Gated Ion Channels in Cancer Cell Proliferation
Cancers 2015, 7(2), 849-875; https://doi.org/10.3390/cancers7020813
Received: 30 March 2015 / Accepted: 12 May 2015 / Published: 22 May 2015
Cited by 43 | PDF Full-text (442 KB) | HTML Full-text | XML Full-text
Abstract
Changes of the electrical charges across the surface cell membrane are absolutely necessary to maintain cellular homeostasis in physiological as well as in pathological conditions. The opening of ion channels alter the charge distribution across the surface membrane as they allow the diffusion [...] Read more.
Changes of the electrical charges across the surface cell membrane are absolutely necessary to maintain cellular homeostasis in physiological as well as in pathological conditions. The opening of ion channels alter the charge distribution across the surface membrane as they allow the diffusion of ions such as K+, Ca++, Cl, Na+. Traditionally, voltage-gated ion channels (VGIC) are known to play fundamental roles in controlling rapid bioelectrical signaling including action potential and/or contraction. However, several investigations have revealed that these classes of proteins can also contribute significantly to cell mitotic biochemical signaling, cell cycle progression, as well as cell volume regulation. All these functions are critically important for cancer cell proliferation. Interestingly, a variety of distinct VGICs are expressed in different cancer cell types, including metastasis but not in the tissues from which these tumors were generated. Given the increasing evidence suggesting that VGIC play a major role in cancer cell biology, in this review we discuss the role of distinct VGIC in cancer cell proliferation and possible therapeutic potential of VIGC pharmacological manipulation. Full article
(This article belongs to the Special Issue Cancer Cell Proliferation)
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