Prognostic significance of STAT3 expression and its correlation with chemoresistance of non-small cell lung cancer cells

Yin, Zhen-Jie; Zhang, Yan; Li, Yu; Lv, Tingting; Liu, Jie; Wang, Xinbo

doi:10.1016/j.acthis.2011.04.002

Cited by 46 publications

(38 citation statements)

References 21 publications

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“…Furthermore, a cooperative induction of HIF‐1 and STAT3 contributes to hypoxia‐mediated immunoresistance in lung cancer cells . Of note, STAT3 and NF‐κB activation promotes chemoresistance and radioresistance in various cancer cell lines, which is akin to that of HIF‐1 …”

Section: Hif‐1 Levels Are Elevated In Tumorsmentioning

confidence: 99%

HIF‐1 at the crossroads of hypoxia, inflammation, and cancer

Balamurugan

2015

Intl Journal of Cancer

468

353

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The complex cross-talk of intricate inter-cellular signaling networks between the tumor and stromal cells promotes cancer progression. Hypoxia is one of the most common conditions encountered within the tumor microenvironment that drives tumor progression. Most responses to hypoxia are elicited by a family of transcription factors called hypoxia-inducible factors (HIFs), which induce expression of a diverse set of genes that assist cells to adapt to hypoxic environments. Among the three HIF protein family members, the role of HIF-1 is well established in cancer progression. HIF-1 functions as a signaling hub to coordinate the activities of many transcription factors and signaling molecules that impact tumorigenesis. This mini review discusses the complex role of HIF-1 and its context-dependent partners under various cancer-promoting events including inflammation and generation of cancer stem cells (CSCs), which are implicated in tumor metastasis and relapse. In addition, the review highlights the importance of therapeutic targeting of HIF-1 for cancer prevention.

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Section: Hif‐1 Levels Are Elevated In Tumorsmentioning

confidence: 99%

HIF‐1 at the crossroads of hypoxia, inflammation, and cancer

Balamurugan

2015

Intl Journal of Cancer

468

353

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“…[8][9][10][11][12][13] Normally, activated STAT protein has a short lifespan, since STAT can be dephosphorylated quickly by protein phosphatases. However, in many primary cancers and cancer cell lines, including lung cancers, STATs (STAT3 and STAT5) are persistently active.…”

Section: Aberrant Activation Of Stat3 In Lung Cancermentioning

confidence: 99%

“…STAT3 may be one of the key oncogenic drivers in NSCLC. [6][7][8][9][10][11][12][13][14] However, several studies have found that STAT3 also plays a role in tumor suppression, [15][16][17][18][19] which should be taken into consideration in cancer therapies based on STAT3 inhibition. In this review, we focus on the molecular function of STAT3.…”

Section: Introductionmentioning

confidence: 99%

Role of STAT3 in lung cancer

Dutta

Sabri

et al. 2014

JAK-STAT

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Lung cancer remains a challenging disease. It is responsible for the high cancer mortality rates in the US and worldwide. Elucidation of the molecular mechanisms operative in lung cancer is an important first step in developing effective therapies. Accumulating evidence over the last 2 decades suggests a critical role for Signal Transducer and Activator of Transcription 3 (STAT3) as a point of convergence for various signaling pathways that are dysregulated in the disease. In this review, we discuss possible molecular mechanisms involving STAT3 in lung tumorigenesis based on recent literature. We consider possible roles of STAT3 in cancer cell proliferation and survival, in the tumor immune environment, and in epigenetic regulation and interaction of STAT3 with other transcription factors. We also discuss the potential role of STAT3 in tumor suppression, which complicates strategies of targeting STAT3 in cancer therapy.

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“…(7, 10). It has been reported that overexpression of STAT3 potentiates growth, survival and radioresistance of NSCLC cells (11). The 5-year overall survival rate of NSCLC patients with high STAT3 expression was significantly lower than that of patients with low STAT3 expression (11), indicating that STAT3 may be an attractive therapeutic target for NSCLC patients.…”

Section: Introductionmentioning

confidence: 99%

Disruption of STAT3 by Niclosamide Reverses Radioresistance of Human Lung Cancer

You

Park

et al. 2014

Molecular Cancer Therapeutics

159

125

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A major challenge affecting the outcomes of patients with lung cancer is the development of acquired radioresistance. However, the mechanisms underlying the development of resistance to therapy are not fully understood. Here we discovered that ionizing radiation (IR) induces phosphorylation of JAK2 and STAT3 in association with increased levels of Bcl2/Bcl-XL in various human lung cancer cells. To uncover new mechanism(s) of radioresistance of lung cancer, we established lung cancer cell model systems with acquired radioresistance. As compared to radiosensitive parental lung cancer cells (i.e. A549, H358 and H157), the JAK2/STAT3/Bcl2/Bcl-XL survival pathway is significantly more activated in acquired radioresistant lung cancer cells (i.e. A549-IRR, H358-IRR and H157-IRR). Higher levels of STAT3 were found to be accumulated in the nucleus of radioresistant lung cancer cells. Niclosamide, a potent STAT3 inhibitor, can reduce STAT3 nuclear localization in radioresistant lung cancer cells. Intriguingly, either inhibition of STAT3 activity by niclosamide or depletion of STAT3 by RNA interference reverses radioresistance in vitro. Niclosamide alone or in combination with radiation overcame radioresistance in lung cancer xenografts. These findings uncover a novel mechanism of radioresistance and provide a more effective approach to overcome radioresistance by blocking the STAT3/Bcl2/Bcl-XL survival signaling pathway, which may potentially improve lung cancer outcome, especially for those patients who have resistance to radiotherapy.

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Prognostic significance of STAT3 expression and its correlation with chemoresistance of non-small cell lung cancer cells

Cited by 46 publications

References 21 publications

HIF‐1 at the crossroads of hypoxia, inflammation, and cancer

HIF‐1 at the crossroads of hypoxia, inflammation, and cancer

Role of STAT3 in lung cancer

Disruption of STAT3 by Niclosamide Reverses Radioresistance of Human Lung Cancer

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