High cofilin-1 levels correlate with cisplatin resistance in lung adenocarcinomas

Becker, Matheus William; Bastiani, Marco Antônio De; Müller, Carolina; Markoski, Melissa Medeiros; Castro, Mauro A. A.; Klamt, Fábio

doi:10.1007/s13277-013-1164-6

Cited by 24 publications

(21 citation statements)

References 31 publications

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“…Indeed, there has been some progress in this area, with emerging evidence confirming that analysis of ERCC1 expression, BRCA mutations and homologous recombination defects maybe useful both prognostically and in predicting response to platinum based regimes [13,14,16,21,96] However, the exploration of alternate biomarkers to predict platinum response is currently in nascent stages. In vitro studies have shown potential links between SULF2 methylation and high cofilin-1 level with cisplatin resistance and steroid receptor co-activator 3 (SRC3) expression with general platinum resistance in ovarian cancer [97][98][99]. Until such biomarkers are comprehensively validated and entrenched into daily oncology practice, the choice of platinum agents still remains at the discretion of the physician.…”

Section: Discussionmentioning

confidence: 99%

Cisplatin versus carboplatin: comparative review of therapeutic management in solid malignancies

Woodward

Coward

2016

Critical Reviews in Oncology/Hematology

231

126

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2 Highlights Platinum analogues, cisplatin and carboplatin, represent some of the most active cytotoxic agents in clinical oncology and are the backbone of most chemotherapeutic regimens  Despite relative similarities in mechanisms of action and activities, there are significant differences in both efficacy and toxicities for both platinum analogues in various malignancies  Carboplatin is a useful alternative in situations where cisplatin is contraindicated and this is not universally at the expense of efficacy  Platinum resistance, both de novo and acquired, is inevitable and understanding the mechanisms of resistance is essential in improving outcomes  Despite the burgeoning era of targeted therapies, the role of efficient DNA damaging agents such as platinum salts remains paramount especially in combination with these novel drugs.3 AbstractThe platinum analogues, cisplatin and carboplatin, are among the most widely used chemotherapeutic agents in oncology. Both agents have a broad spectrum of clinical activity in numerous malignancies including gynaecological cancers, germ cell tumours, head and neck cancer, thoracic cancers and bladder cancer. Although the final mechanism of inducing tumour cell apoptosis is similar for both compounds, cisplatin has been shown to be more effective in treating specific tumour types. Whilst more favourable toxicity profiles are often associated with carboplatin, this can frequently translate to inferior response in certain malignancies. This review succinctly collates the evidence for the preferential use of these platinum analogues in particular settings in addition to the long-standing dilemma surrounding the paucity of biomarkers predicting response to these agents.

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Section: Discussionmentioning

confidence: 99%

Cisplatin versus carboplatin: comparative review of therapeutic management in solid malignancies

Woodward

Coward

2016

Critical Reviews in Oncology/Hematology

231

126

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“…In non-small cell lung cancer (NSCLC), high cofilin-1 levels were correlated with lower overall survival rate, cellular invasiveness and resistance to drugs, and particularly, to cisplatin (30)(31)(32)(33). Coflin-1 was also found upregulated in breast cancer and its levels correlated with tumor size and stage (34)(35)(36).…”

Section: Discussionmentioning

confidence: 99%

Proteomic Analysis of Normal and Cancer Cervical Cell Lines Reveals Deregulation of Cytoskeleton-associated Proteins

2017

CGP

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Cervical cancer represents the fourth most common and fatal form of cancer among women worldwide (1). More than 90% of cervical cancer cases arise as a consequence of a human papilloma virus (HPV) infection. Currently, 210 different HPV types have been officially recognized (2), and -based on their carcinogenic potential -have been classified either as low-risk HPV types, or as high-risk and potentially carcinogenic (3). Of the high-risk group, the five most common HPV types include HPV 16, 18, 45, 30, and 33, while types 16 and 18 alone, account for about 70% of all cervical cancer cases (4).In the early phase of cervical carcinogenesis, HPV initially infects the proliferating cells of the basal layer of the cervical stratified epithelium through abrasions of the mucosal epithelium. Following infection, the HPV genome remains in the form of nuclear extrachromosomal episome, and due to the repression of the viral E6 and E7 oncoprotein synthesis, the viral DNA replication occurs at very low levels (5). Following the gradual differentiation of the basal cells and their migration to the upper layers of the epithelium, an increased expression of E6 and E7 oncoproteins occurs, leading to inhibition of apoptosis, while the viral genome is replicated further. At this point, structural proteins and mature viral particles are produced, and the shed virus can then initiate a new infection. These 253 This article is freely accessible online.

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“…Recent studies demonstrated that high-expression levels of cofilin-1 in many cancers correlated with invasion and metastasis, chemotherapy resistance, and poor prognosis [4, 6, 31–33]. The mammalian cofilin-encoding gene encodes two members of the actin-binding protein family: cofilin-1, which is expressed in various nonmuscle tissues, and cofilin-2, which is mainly expressed in muscle tissue [34].…”

Section: Discussionmentioning

confidence: 99%

“…In another study, p-cofilin-1 also showed high-expression levels in vincristine-resistant human osteosarcoma cell line MG63/VCR, which was upregulated by overexpression of LIMK1 [5]. The cofilin-1 was showed higher expression levels in DDP-resistant non-small cell lung cancer (NSCLC) cell ICR-A549 [6]. Cofilin-1 belongs to the actin-binding protein family, the members of which regulate actin depolymerisation.…”

Section: Introductionmentioning

confidence: 99%

The Zuo Jin Wan Formula Induces Mitochondrial Apoptosis of Cisplatin-Resistant Gastric Cancer Cells via Cofilin-1

Tang

Sun

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Despite the status of cisplatin (DDP) as a classical chemotherapeutic agent in the treatment of cancer, the development of multidrug resistance often leads to a failure of DDP therapy. Here we found that phosphorylated cofilin-1 (p-cofilin-1) was overexpressed in the DDP-resistant human gastric cancer cell lines SGC7901/DDP and BGC823/DDP, relative to the respective parent cell lines (SGC7901 and BGC823), and that DDP induced the dephosphorylation of p-cofilin-1 in both parent lines but not in the DDP-resistant lines. However, we noted that the traditional Chinese medicine formula Zuo Jin Wan (ZJW) could induce the dephosphorylation of p-cofilin-1 and promote cofilin-1 translocation from the cytoplasm into the mitochondria in both SGC7901/DDP and BGC823/DDP cells. This mitochondrial translocation of cofilin-1 was found to induce the conversion of filamentous actin to globular-actin, activate mitochondrial damage and calcium overloading, and induce the mitochondrial apoptosis pathway. We further observed that these effects of ZJW on DDP-resistant human gastric cancer cell lines could be reversed via transfection with cofilin-1-specific siRNA, or treatment with a PP1 and PP2A inhibitor. These results suggest that ZJW is an effective drug therapy for patients with DDP-resistant gastric cancer.

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High cofilin-1 levels correlate with cisplatin resistance in lung adenocarcinomas

Cited by 24 publications

References 31 publications

Cisplatin versus carboplatin: comparative review of therapeutic management in solid malignancies

Cisplatin versus carboplatin: comparative review of therapeutic management in solid malignancies

Proteomic Analysis of Normal and Cancer Cervical Cell Lines Reveals Deregulation of Cytoskeleton-associated Proteins

The Zuo Jin Wan Formula Induces Mitochondrial Apoptosis of Cisplatin-Resistant Gastric Cancer Cells via Cofilin-1

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