Radiation-induced Cancer Cell Repopulation: A Possible Mechanism Implied by Experiments Using Transplantable Mouse-derived Sarcoma Cell Line

Nishioka, Takeshi; Yasuda, Motoaki; Takeshima, Tsuguhide; Haga, Hisashi; Miyai, Yusuke; Shibata, Ken Ichiro; Yamazaki, Rie; Shirato, Hiroki; Teduka, Masahiro; Date, Hiroyuki

doi:10.1247/csf.10008

Cited by 6 publications

(7 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cancer cells that survive after irradiation acquire malignant phenotypes [2–5]. We previously reported that P cells that survive after irradiation (IR cells) are more invasive than non-irradiated P cells [6–8].…”

Section: Resultsmentioning

confidence: 99%

“…However, some cancer cells survive after irradiation and repopulate tumors with highly malignant phenotypes, such as high proliferative ability and invasiveness, which correlate with poor prognosis [2–5]. As shown in our previous studies, lung cancer cells that survive irradiation acquire invasive ability that is dependent on cell-matrix adhesion regulated by integrin β1, cellular contractile force modulated by myosin regulatory light chain (MRLC), and molecular signaling mediated by epidermal growth factor receptor and other molecules [6–8].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Activating transcription factor 5 enhances radioresistance and malignancy in cancer cells

et al. 2015

Self Cite

View full text Add to dashboard Cite

Radiotherapy is effective for treating various types of tumors. However, some cancer cells survive after irradiation and repopulate tumors with highly malignant phenotypes that correlate with poor prognosis. It is not known how cancer cells survive and generate malignant tumors after irradiation. Here, we show that activating transcription factor 5 (ATF5) promotes radioresistance and malignancy in cancer cells after irradiation. In the G1-S phase of the cell cycle, cancer cells express high levels of ATF5, which promotes cell cycle progression and thereby increases radioresistance. Furthermore, ATF5 increases malignant phenotypes, such as cell growth and invasiveness, in cancer cells in vitro and in vivo. We have identified a new mechanism for the regeneration of highly malignant tumors after irradiation and shown that ATF5 plays a key role in the process.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Activating transcription factor 5 enhances radioresistance and malignancy in cancer cells

et al. 2015

Self Cite

View full text Add to dashboard Cite

show abstract

“…Tumor cell repopulation is a key process causing tumor relapse during cancer chemotherapy or radiotherapy [13]. Repopulation of surviving tumor cells can occur between dose fractions of either radiation or chemotherapy and can lead to treatment failure [14].…”

Section: Discussionmentioning

confidence: 99%

Sonic Hedgehog Signaling Pathway Supports Cancer Cell Growth during Cancer Radiotherapy

Tian

Cheng

et al. 2013

PLoS ONE

View full text Add to dashboard Cite

Tumor growth after radiotherapy is a commonly recognized cause of therapeutic failure. In this way, we examined tumor cell growth after radiotherapy by establishing a cancer cell growth model in vitro. We accomplished this model by seeding non-irradiated firefly luciferase2 and green fluorescent protein fusion gene (Fluc) labeled living cancer reporter cells onto a feeder layer of irradiated cancer cells. The living tumor cell growth was monitored by bioluminescence imaging. The living reporter cells grew faster when seeded onto lethally irradiated feeder cells than when seeded onto non-irradiated feeder cells or when seeded in the absence of feeder cells. We found that the expression levels of the Shh and Gli1 proteins, both of which are critical proteins in Sonic hedgehog (SHH) signaling, were increased after irradiation and that this expression was positively correlated with reporter cell growth. Moreover, the dying cell stimulation of living tumor cell growth was enhanced by the addition of SHH signaling agonists and inhibited by SHH signaling antagonists. SHH agonists also enhanced reporter cell growth in the absence of irradiated feeder cells, suggesting this mechanism plays a role in feeder cell growth stimulation. Given these results, we conclude that SHH signaling activation plays an important role during tumor repopulation after radiotherapy.

show abstract

“…Tumor necrosis Factor-α (TNF-α) also stimulates LOX expression (Voloshenyuk et al, 2011b). It is interesting that our irradiation-surviving cells expressed higher IL6-(36.0-fold) and LOX-mRNA (4.8-fold) compared to un-irradiated parental cells in vitro (Nishioka et al, 2011). IL6 might have an influence on LOX expression.…”

Section: Introduction and Molecular Biology Of Loxmentioning

confidence: 90%

Lysyl Oxidase: From Basic Science to Future Cancer Treatment

Nishioka

Eustace

West

2012

Cell Struct. Funct.

Self Cite

View full text Add to dashboard Cite

ABSTRACT. In this mini-review, we discuss the physiological and pathological roles of lysyl oxidase (LOX) and its family, LOX-like proteins (LOXL), in relation to prognosis of major cancers. The number of reports on LOX family is numerous. We have decided to review the articles that were recently published (i.e. past 5 years). Experimental techniques in molecular biology have advanced surprisingly in the past decade. Accordingly, the results of the studies are more reliable. Most studies reached the same conclusion; a higher LOX-or LOXLexpression is associated with a poor prognosis. Molecular experiments have already started aiming for clinical application, and the results are encouraging. Suppressing LOX or LOXL activities resulted in lower cell motility in collagen gel and, moreover, succeeded in reducing metastases in mice. LOX family members were originally recognized as molecules that cross-link collagen fibers in the extracellular matrix. Recent studies demonstrated that they are also involved in a phenomenon called Epithelial Mesenchymal Transition (EMT). This may affect cell movement and cancer cell invasiveness. LOX and LOXL2 are regulated by hypoxia, a major factor in the failure of cancer treatment. Here we discuss the molecular biology of the LOX family in relation to its role in tumor biology.

show abstract

Radiation-induced Cancer Cell Repopulation: A Possible Mechanism Implied by Experiments Using Transplantable Mouse-derived Sarcoma Cell Line

Cited by 6 publications

References 16 publications

Activating transcription factor 5 enhances radioresistance and malignancy in cancer cells

Activating transcription factor 5 enhances radioresistance and malignancy in cancer cells

Sonic Hedgehog Signaling Pathway Supports Cancer Cell Growth during Cancer Radiotherapy

Lysyl Oxidase: From Basic Science to Future Cancer Treatment

Contact Info

Product

Resources

About