Expression and prognostic relevance of STAT3 and cyclin D1 in non-small cell lung cancer

Ai, Ting; Wang, Zhouquan; Zhang, Mingxin; Zhang, Lingmin; Wang, Ning; Li, Weiwei; Song, Liping

doi:10.5301/jbm.2012.9146

Cited by 24 publications

(23 citation statements)

References 21 publications

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“…Thus, the JAK2/STAT3 pathway is an important therapeutic target for cancer treatment. Moreover, there is a significant association between the JAK2/STAT3 pathway and lung tumor development in the patient [49,50]. Our previous studies demonstrated that bee venom and melittin inhibited the JAK2/ STAT3 pathway, resulting in lung cancer cell growth inhibition [51].…”

Section: Discussionmentioning

confidence: 98%

PRDX6 promotes tumor development via the JAK2/STAT3 pathway in a urethane-induced lung tumor model

Yun

Park

et al. 2015

Free Radical Biology and Medicine

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Section: Discussionmentioning

confidence: 98%

PRDX6 promotes tumor development via the JAK2/STAT3 pathway in a urethane-induced lung tumor model

Yun

Park

et al. 2015

Free Radical Biology and Medicine

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“…The c-Myc oncoprotein promotes cell cycling progression, plays a vital role in most human cancers (Dang et al , 2006) and cooperates with Mcl-1 in the development of NSCLC (Allen et al ., 2011). Similarly, cyclin D1 is a central player in the cell cycle and plays an essential role in the development of NSCLC (Ai et al ., 2012). Consequently, the down-regulation of Bcl-2, Bclx L , Mcl-1, Survivin, c-Myc and cyclin D1 by CAERS imply that this extract could effectively target the survival advantage provided by these effectors.…”

Section: Discussionmentioning

confidence: 99%

Crude alkaloid extract of Rhazya stricta inhibits cell growth and sensitizes human lung cancer cells to cisplatin through induction of apoptosis

Elkady

2013

Genet. Mol. Biol.

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There is an urgent need to improve the clinical management of non-small cell lung cancer (NSCLC), one of the most frequent causes of cancer-related deaths in men and women worldwide. Rhazya stricta, an important medicinal plant used in traditional Oriental medicine, possesses anti-oxidant, anti-carcinogenic and free radical scavenging properties. This study was done to explore the potential anticancer activity of a crude alkaloid extract of R. stricta (CAERS) against the NSCLC line A549. CAERS markedly suppressed the growth of A549 cells and considerably enhanced the anti-proliferative potential of cisplatin. CAERS-mediated inhibition of A549 cell growth correlated with the induction of apoptosis that was accompanied by numerous morphological changes, DNA fragmentation, an increase in the Bax/Bcl-2 ratio, the release of mitochondrial cytochrome c, activation of caspases 3 and 9 and cleavage of poly(ADP-ribose)-polymerase. CAERS reduced the constitutive expression of anti-apoptotic proteins (Bcl-2, Bcl-XL, Mcl-1 and Survivin) and cell cycle regulating proteins (cyclin D1 and c-Myc), but enhanced expression of the proapoptotic proteins Noxa and BAD. These observations indicate that CAERS induced apoptosis and sensitized NSCLC to cisplatin via a mitochondria-mediated apoptotic pathway. These data provide a rationale for using a combination of CAERS and CDDP to treat NSCLC and other CDDP-resistant tumors.

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“…It has been shown that upregulated expression of STAT3 is associated with more malignant behavior of tumor cells and worse prognosis in a variety of human malignancies, e.g., cancers of the breast, prostate, ovary, lung, head and neck, esophagus, and brain [53,54,55,56,57,58,59,60,61]. In pancreatic cancer, STAT3 was shown to regulate angiogenesis and metastasis [62] and to promote cellular proliferation by accelerating G1/S-phase progression [63].…”

Section: Jak/stat Signaling In Different Cancer Typesmentioning

confidence: 99%

The Role of STAT3 in Thyroid Cancer

Sosonkina

Starenki

Park

2014

Cancers

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Thyroid cancer is the most common endocrine malignancy and its global incidence rates are rapidly increasing. Although the mortality of thyroid cancer is relatively low, its rate of recurrence or persistence is relatively high, contributing to incurability and morbidity of the disease. Thyroid cancer is mainly treated by surgery and radioiodine remnant ablation, which is effective only for non-metastasized primary tumors. Therefore, better understanding of the molecular targets available in this tumor is necessary. Similarly to many other tumor types, oncogenic molecular alterations in thyroid epithelium include aberrant signal transduction of the mitogen-activated protein kinase, phosphatidylinositol 3-kinase/AKT (also known as protein kinase B), NF-кB, and WNT/β-catenin pathways. However, the role of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT3) pathway, a well-known mediator of tumorigenesis in different tumor types, is relatively less understood in thyroid cancer. Intriguingly, recent studies have demonstrated that, in thyroid cancer, the JAK/STAT3 pathway may function in the context of tumor suppression rather than promoting tumorigenesis. In this review, we provide an update of STAT3 function in thyroid cancer and discuss some of the evidences that support this hypothesis.

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Expression and prognostic relevance of STAT3 and cyclin D1 in non-small cell lung cancer

Cited by 24 publications

References 21 publications

PRDX6 promotes tumor development via the JAK2/STAT3 pathway in a urethane-induced lung tumor model

PRDX6 promotes tumor development via the JAK2/STAT3 pathway in a urethane-induced lung tumor model

Crude alkaloid extract of Rhazya stricta inhibits cell growth and sensitizes human lung cancer cells to cisplatin through induction of apoptosis

The Role of STAT3 in Thyroid Cancer

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