Suppression of Nrf2-driven heme oxygenase-1 enhances the chemosensitivity of lung cancer A549 cells toward cisplatin

Kim, Hak-Ryul; Kim, Se-Jin; Kim, Eun-Jung; Park, Jung Hyun; Yang, Sei‐Hoon; Jeong, Eun Taik; Park, Channy; Youn, Myung-Ja; So, Hong-Seob; Park, Raekil

doi:10.1016/j.lungcan.2007.09.021

Cited by 99 publications

(82 citation statements)

References 39 publications

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“…In addition, there is increased expression of HO-1 in a variety of cancers including brain tumors [16], an event that may antagonize ROS inducers' therapeutic potentials. Indeed, inhibition of the Nrf2-HO-1 pathway augmented ROS generation and cell death induced by cisplatin in lung cancer cells [17]. Therefore, these facts support the rationale that abrogation of HO-1 may enhance the anti-cancer effects of ROS inducers on glioma.…”

Section: Introductionmentioning

confidence: 66%

Inhibition of heme oxygenase-1 enhances anti-cancer effects of arsenic trioxide on glioma cells

et al. 2011

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We have previously reported that arsenic trioxide (ATO) could inhibit glioma growth both in vitro and in vivo, and demonstrated its potent therapeutic effects on gliomas. In this study we showed that ATO induced cell damage and heme oxygenase-1 (HO-1) expression in glioma cells via ROS generation. HO-1 inducer clearly protected from ATO-induced cell death and ROS generation, and HO-1 inhibitor led to a significant increase in cell death and ROS generation induced by ATO. In addition, knockdown of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) strongly inhibited HO-1 expression induced by ATO, and significantly enhanced ATO-induced oxidative damage. Our results demonstrated, for the first time, that HO-1 inhibition or Nrf2 knockdown significantly potentiated ATO's effects on glioma cells. Considering that HO-1 is highly expressed in glioma tissues, administration of ATO in combination with either HO-1 inhibitor or Nrf2 knockdown may act as a new approach to the treatment of glioma.

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Section: Introductionmentioning

confidence: 66%

Inhibition of heme oxygenase-1 enhances anti-cancer effects of arsenic trioxide on glioma cells

et al. 2011

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“…Therefore, recent studies have suggested modulation of Nrf2 as a promising strategy for anticancer therapy. Silencing Nrf2 or HO-1 with small interfering RNA (siRNA) has been shown to increase the efficacy of chemotherapy in NSCLC cells in vitro and in vivo [23][24][25]. In accord with these results, the chemosensitivity of A549 cells to cisplatin is enhanced by inhibition of HO-1 with zinc protoporphyrin, a specific HO-1 inhibitor [25], or inhibition of cisplatininduced HO-1 expression by AG1478, an epidermal growth factor receptor inhibitor [26].…”

Section: Discussionmentioning

confidence: 89%

An effective strategy for increasing the radiosensitivity of Human lung Cancer cells by blocking Nrf2-dependent antioxidant responses

Lee

Lim

Kim

et al. 2012

Free Radical Biology and Medicine

108

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“…Additional pathway has been proposed in case of AML cells; HO-1 counteracted induction of apoptosis caused by NFjB inhibition (176) and provided resistance to TNFa-induced cell death (177). Importantly, many cytoprotective effects ascribed to Nrf-2 were shown to be dependent on HO-1 activation (96,134).…”

Section: Ho-1 Role In Cancer Scsmentioning

confidence: 99%

Role of Heme Oxygenase-1 in Postnatal Differentiation of Stem Cells: A Possible Cross-Talk with MicroRNAs

Kozakowska

Szade

Dulak

et al. 2014

Antioxidants & Redox Signaling

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Significance: Heme oxygenase-1 (HO-1) converts heme to biliverdin, carbon monoxide, and ferrous ions, but its cellular functions are far beyond heme metabolism. HO-1 via heme removal and degradation products acts as a cytoprotective, anti-inflammatory, immunomodulatory, and proangiogenic protein, regulating also a cell cycle. Additionally, HO-1 can translocate to nucleus and regulate transcription factors, so it can also act independently of enzymatic function. Recent Advances: Recently, a body of evidence has emerged indicating a role for HO-1 in postnatal differentiation of stem and progenitor cells. Maturation of satellite cells, skeletal myoblasts, adipocytes, and osteoclasts is inhibited by HO-1, whereas neurogenic differentiation and formation of cardiomyocytes perhaps can be enhanced. Moreover, HO-1 influences a lineage commitment in pluripotent stem cells and maturation of hematopoietic cells. It may play a role in development of osteoblasts, but descriptions of its exact effects are inconsistent. Critical Issues: In this review we discuss a role of HO-1 in cell differentiation, and possible HO-1-dependent signal transduction pathways. Among the potential mediators, we focused on microRNA (miRNA). These small, noncoding RNAs are critical for cell differentiation. Recently we have found that HO-1 not only influences expression of specific miRNAs but also regulates miRNA processing enzymes. Future Directions: It seems that interplay between HO-1 and miRNAs may be important in regulating fates of stem and progenitor cells and needs further intensive studies.

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Suppression of Nrf2-driven heme oxygenase-1 enhances the chemosensitivity of lung cancer A549 cells toward cisplatin

Cited by 99 publications

References 39 publications

Inhibition of heme oxygenase-1 enhances anti-cancer effects of arsenic trioxide on glioma cells

Inhibition of heme oxygenase-1 enhances anti-cancer effects of arsenic trioxide on glioma cells

An effective strategy for increasing the radiosensitivity of Human lung Cancer cells by blocking Nrf2-dependent antioxidant responses

Role of Heme Oxygenase-1 in Postnatal Differentiation of Stem Cells: A Possible Cross-Talk with MicroRNAs

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