&lt;p&gt;Anti-Angiogenic Therapy in the Treatment of Non-Small Cell Lung Cancer&lt;/p&gt;

Tian, Wentao; Cao, Chenghui; Shu, Long; Wu, Fang

doi:10.2147/ott.s276150

Cited by 31 publications

(29 citation statements)

References 97 publications

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“…A major consequence of EGFR signaling in hypoxic tumors appears to be an enhanced induction of vascular endothelial growth factor (VEGF); and the molecular mechanisms underlying the link between EGFR signaling and VEGF expression include both HIF-1α–dependent and independent mechanisms. VEGF, a HIF-1α target gene, is modulated by activation of several receptor tyrosine kinases, and EGFR inhibition has been found to decrease VEGF expression in many tumor types ( 44 ). HIF-1α transcriptionally regulates VEGF expression and binds directly to the hypoxia-response elements in the promoters of the VEGF-regulated genes.…”

Section: Hypoxia-induced Chemotherapy Resistance In Nsclcmentioning

confidence: 99%

SIRT1/PGC-1α/PPAR-γ Correlate With Hypoxia-Induced Chemoresistance in Non-Small Cell Lung Cancer

Luo

et al. 2021

Front. Oncol.

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Resistance is the major cause of treatment failure and disease progression in non-small cell lung cancer (NSCLC). There is evidence that hypoxia is a key microenvironmental stress associated with resistance to cisplatin, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), and immunotherapy in solid NSCLCs. Numerous studies have contributed to delineating the mechanisms underlying drug resistance in NSCLC; nevertheless, the mechanisms involved in the resistance associated with hypoxia-induced molecular metabolic adaptations in the microenvironment of NSCLC remain unclear. Studies have highlighted the importance of posttranslational regulation of molecular mediators in the control of mitochondrial function in response to hypoxia-induced metabolic adaptations. Hypoxia can upregulate the expression of sirtuin 1 (SIRT1) in a hypoxia-inducible factor (HIF)-dependent manner. SIRT1 is a stress-dependent metabolic sensor that can deacetylate some key transcriptional factors in both metabolism dependent and independent metabolic pathways such as HIF-1α, peroxisome proliferator-activated receptor gamma (PPAR-γ), and PPAR-gamma coactivator 1-alpha (PGC-1α) to affect mitochondrial function and biogenesis, which has a role in hypoxia-induced chemoresistance in NSCLC. Moreover, SIRT1 and HIF-1α can regulate both innate and adaptive immune responses through metabolism-dependent and -independent ways. The objective of this review is to delineate a possible SIRT1/PGC-1α/PPAR-γ signaling-related molecular metabolic mechanism underlying hypoxia-induced chemotherapy resistance in the NSCLC microenvironment. Targeting hypoxia-related metabolic adaptation may be an attractive therapeutic strategy for overcoming chemoresistance in NSCLC.

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Section: Hypoxia-induced Chemotherapy Resistance In Nsclcmentioning

confidence: 99%

SIRT1/PGC-1α/PPAR-γ Correlate With Hypoxia-Induced Chemoresistance in Non-Small Cell Lung Cancer

Luo

et al. 2021

Front. Oncol.

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“…Nevertheless, according to our findings, anlotinib may still be an appropriate choice for patients with advanced age, poor PS, or reluctance to receive chemotherapy. Anti-angiogenesis therapy can normalize abnormal vascularization in tumors, improve delivery of anti-tumor agents (Alshangiti et al 2018), modify the immunosuppressive microenvironment, and crosslink with the EGFR signaling pathway (Tian et al 2020); and thus play a synergistic antitumor role when combined with other treatments including chemotherapy, EGFR/TKIs, and ICIs. Additionally, the good tolerance and non-overlapping toxicity spectrum of anlotinib makes it possible to be combined.…”

Section: Discussionmentioning

confidence: 99%

The real-world efficacy and safety of anlotinib in advanced non-small cell lung cancer

Wang

Jin

Cheng

et al. 2021

J Cancer Res Clin Oncol

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Purpose Anlotinib is an anti-angiogenetic multi-targeted tyrosine kinase inhibitor. This study aimed to evaluate the efficacy and safety of anlotinib in advanced non-small cell lung cancer (aNSCLC) in the real world. Methods Patients with aNSCLC receiving anlotinib were enrolled in two cohorts (treatment naive and previously treated). The endpoints included progression-free survival (PFS), overall survival (OS) and anlotinib-related adverse events (ar-AEs). Results 203 patients accrued in the study. In the treatment-naïve cohort (n = 80), the PFS was 7.4 (95% confidence interval [CI] 4.1-10.7) and OS was 10.8 (95% CI 5.8-15.8) months of monotherapy group (immature survival for combination group). In previously treated cohort (n = 123), the PFS was 8.0 months (95% CI 6.1-9.9) in the combination group and 4.3 months (95% CI 2.1-6.6) in the monotherapy group (hazard ratio [HR] 0.49; 95% CI 0.29-0.83; p = 0.007), respectively. The OS was 18.5 months (95% CI 10.5-26.6) in the combination group and 7.8 months (95% CI 7.1-8.4) in the monotherapy group (HR 0.38; 95% CI 0.22-0.66; p = 0.001), respectively. The ar-AEs of grade ≥ 3 in the monotherapy and the combination groups were hypertension (9.0 and 8.7%), fatigue (8.1 and 7.6%), hand-foot syndrome (8.1 and 6.5%), diarrhea (5.4 and 8.7%), proteinuria (5.4 and 5.4%), and mucositis oral (6.3 and 8.7%). Conclusion In aNSCLC, anlotinib monotherapy has a promising efficacy in the first-line setting. It may be an option for those who are ineligible for chemotherapy; anlotinib combination therapy in a ≥ second-line setting showed manageable toxicities and encouraging efficacy, indicating a good application prospect. Trial registration This study was retrospectively registered with ISRCTN Registry (ID ISRCTN35543977) on January 26th, 2021 and Chinese Clinical Trial Register (ChiCTR2000032265) on April 4th, 2020.

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“…Hence, this process plays a key role in tumor progression and is now recognized as one of the hallmarks of cancer [ 224 , 225 ]. Vascular endothelial growth factor (VEGF) is an essential factor for vascular endothelial cells; its expression is up-regulated in most cancers, and its crucial role in tumor angiogenesis is well defined [ 226 , 227 , 228 , 229 , 230 , 231 ]. Among the VEGF isoforms, VEGF-A was shown to play a key role in PCa angiogenesis [ 232 , 233 , 234 ].…”

Section: The Gnrh/gnrh-r Axis In Crpcmentioning

confidence: 99%

Dissecting the Hormonal Signaling Landscape in Castration-Resistant Prostate Cancer

Fontana

Limonta

2021

Cells

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Understanding the molecular mechanisms underlying prostate cancer (PCa) progression towards its most aggressive, castration-resistant (CRPC) stage is urgently needed to improve the therapeutic options for this almost incurable pathology. Interestingly, CRPC is known to be characterized by a peculiar hormonal landscape. It is now well established that the androgen/androgen receptor (AR) axis is still active in CRPC cells. The persistent activity of this axis in PCa progression has been shown to be related to different mechanisms, such as intratumoral androgen synthesis, AR amplification and mutations, AR mRNA alternative splicing, increased expression/activity of AR-related transcription factors and coregulators. The hypothalamic gonadotropin-releasing hormone (GnRH), by binding to its specific receptors (GnRH-Rs) at the pituitary level, plays a pivotal role in the regulation of the reproductive functions. GnRH and GnRH-R are also expressed in different types of tumors, including PCa. Specifically, it has been demonstrated that, in CRPC cells, the activation of GnRH-Rs is associated with a significant antiproliferative/proapoptotic, antimetastatic and antiangiogenic activity. This antitumor activity is mainly mediated by the GnRH-R-associated Gαi/cAMP signaling pathway. In this review, we dissect the molecular mechanisms underlying the role of the androgen/AR and GnRH/GnRH-R axes in CRPC progression and the possible therapeutic implications.

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<p>Anti-Angiogenic Therapy in the Treatment of Non-Small Cell Lung Cancer</p>

Cited by 31 publications

References 97 publications

SIRT1/PGC-1α/PPAR-γ Correlate With Hypoxia-Induced Chemoresistance in Non-Small Cell Lung Cancer

SIRT1/PGC-1α/PPAR-γ Correlate With Hypoxia-Induced Chemoresistance in Non-Small Cell Lung Cancer

The real-world efficacy and safety of anlotinib in advanced non-small cell lung cancer

Dissecting the Hormonal Signaling Landscape in Castration-Resistant Prostate Cancer

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