Current views on molecularly targeted therapy for lung cancer – a review of literature from the last five years

Rybarczyk-Kasiuchnicz, Agnieszka

doi:10.5114/kitp.2018.76478

Cited by 6 publications

(4 citation statements)

References 38 publications

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“…Traditionally, clinical methods, including surgery, chemotherapy or a combination are the primary treatment approaches for lung cancer. Recently, molecular-targeted drugs ( 4 ), anti-angiogenic therapy ( 5 ) and cancer immunotherapy ( 6 ) have been widely applied in patients with lung cancer. Despite advances in early diagnosis and standard treatment, the overall 5-year survival rate for NSCLC is <15% ( 7 ), and there is an urgent requirement for the development of novel therapeutic approaches for NSCLC.…”

Section: Introductionmentioning

confidence: 99%

Pectolinarigenin inhibits non‑small cell lung cancer progression by regulating the PTEN/PI3K/AKT signaling pathway

Gao

Pan

2018

Oncol Rep

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Lung cancer is the principal cause of cancer-associated mortality. Pectolinarigenin (Pec) reportedly has effective antitumor activity against certain cancer types. Phosphatase and tensin homolog (PTEN) is a well-known tumor suppressor and serves a vital role in cancer progression. However, the effect of Pec on non-small cell lung cancer (NSCLC) cell proliferation and metastasis, and the underlying mechanism, has not yet been elucidated. In the present study, it was demonstrated that Pec inhibited the proliferation of A549 and Calu-3 cells in dose- and time-dependent manners. The apoptosis rate significantly increased with increasing doses of Pec. Apoptosis-associated protein expression was additionally altered by Pec exposure. Pec was able to suppress the metastasis of NSCLC cells; it upregulated the mRNA and protein expression levels of E-cadherin, and downregulated the mRNA and protein expression levels of vimentin. Additionally, Pec was able to activate PTEN and subsequently downregulate the PI3K/protein kinase B (AKT) signaling pathway. In summary, Pec was able to inhibit cell proliferation, promote apoptosis and suppress metastasis in NSCLC cells through the PTEN/PI3K/AKT signaling pathway, indicating that Pec is a potential agent for NSCLC therapy.

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Section: Introductionmentioning

confidence: 99%

Pectolinarigenin inhibits non‑small cell lung cancer progression by regulating the PTEN/PI3K/AKT signaling pathway

Gao

Pan

2018

Oncol Rep

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“…Several lines of evidence supported critical roles for Hedgehog and MAPK signaling in lung cancer [16]. Accordingly, there was a growing interest in studying Hedgehog and MAPK pathways via their co-targeting by GANT61 (an inhibitor of downstream targets of Hh pathway) and BI-847325 (a dual MEK and Aurora kinase inhibitor).…”

Section: Discussionmentioning

confidence: 99%

GANT61/BI-847325 combination: a new hope in lung cancer treatment

et al. 2022

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Despite the huge efforts employed to implement novel chemotherapeutic paradigms for lung cancer, the disease still remains a major concern worldwide. Targeting molecular pathways as Hedgehog (Hh) and Mitogen-activated protein kinase (MAPK) represent a new hope in lung cancer treatment. This work was undertaken to evaluate the antitumor effects of GANT61 (5 μM), BI-847325(30 μM), and GANT61 (5 μM)/BI-847325(30 μM) combination on A549 adenocarcinoma lung cancer cell line. The growth inhibition 50 (GI50) for both drugs was performed using MTT. The protein levels of Caspase-3, Bcl-2-associated X protein (Bax), Myeloid cell leukemia sequence 1 (MCL-1), cyclin D1, vascular endothelial growth factor (VEGF), extracellular signal-regulated kinases (ERK), p-Akt, and phosphohistone H3 (pHH3) were measured using ELISA. Glioma-associated oncogene homolog 1(Gli1) gene expression was assessed by quantitative real-time PCR. The GI50 for GANT61 and BI-8473255 were 5 µM and 30 µM, respectively. Caspase-3 and Bax protein levels were significantly elevated while MCL-1, cyclin D1, VEGF, ERK 1/2, p-Akt, and pHH3 levels were significantly reduced by both drugs and their combination relative to the control group. Gli1 gene expression was down-regulated in all groups relative to the control group. GANT61, BI-847325 and their combination inhibited proliferation and angiogenesis but activated the apoptotic pathway. Both drugs conferred a profound negative impact on the crosstalk between each of Hh and MAPK pathways and Phosphoinositide 3 -kinases (PI3K)/Akt/Mammalian target of Rapamycin (mTOR). To the best of our knowledge, the antitumor effects of BI-847325/GANT61 combination have not been tested before. Further in-vitro and in-vivo studies are warranted to support the findings.

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“…The presence of these activating mutations is the therapeutic target for the lowmolecular-weight selective inhibitor of the ALK and ROS1 tyrosine kinase receptors -crizotinib. 29 BRAF is a member of the serine/threonine kinase RAF family that is regulated by binding to RAS and directly activating MEK1/2, which can further phosphorylate ERK1/2. BRAF mutations are detected in approximately 2% to 4% of lung cancer, mainly adenocarcinomas.…”

Section: Nsclc Molecular Targeted Therapymentioning

confidence: 99%

Novel platinum agents and mesenchymal stromal cells for thoracic malignancies: state of the art and future perspectives

Petrella

Rimoldi

Facchetti

et al. 2018

Expert Opinion on Therapeutic Patents

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Current views on molecularly targeted therapy for lung cancer – a review of literature from the last five years

Cited by 6 publications

References 38 publications

Pectolinarigenin inhibits non‑small cell lung cancer progression by regulating the PTEN/PI3K/AKT signaling pathway

Pectolinarigenin inhibits non‑small cell lung cancer progression by regulating the PTEN/PI3K/AKT signaling pathway

GANT61/BI-847325 combination: a new hope in lung cancer treatment

Novel platinum agents and mesenchymal stromal cells for thoracic malignancies: state of the art and future perspectives

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