Docetaxel-loaded D-α-tocopheryl polyethylene glycol-1000 succinate liposomes improve lung cancer chemotherapy and reverse multidrug resistance

Li, Na; Mai, Yaping; Liu, Qiang; Gou, Guojing; Yang, Jianhong

doi:10.1007/s13346-020-00720-9

Cited by 33 publications

(14 citation statements)

References 47 publications

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“…Lung cancer is the leading cause of cancer-related death worldwide ( 25 ). Multiple pharmacogenomic molecular alterations can lead to chemoresistance in lung cancer cells, such as the augmented expression of tubulin III, stathmin, and ribonucleotide reductase, and the uridine diphosphate glucuronosyltransferase isoform 1A1 genotype is associated with the treatment failure of irinotecan ( 26 – 28 ). It has been found that nicotine can induce resistance to chemotherapy and radiation in a number of tumors by activating a range of intracellular signaling pathways and promoting angiogenesis ( 29 , 30 ).…”

Section: Discussionmentioning

confidence: 99%

Nicotine‑induced miR‑21‑3p promotes chemoresistance in lung cancer by negatively regulating FOXO3a

et al. 2022

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Lung cancer is the leading cause of cancer-related mortality worldwide and cigarette smoking is reported to contribute to the lung cancer-related mortality. The present study aimed to investigate the molecular mechanism underlying nicotine-induced chemoresistance in lung cancer. The expression of microRNA (miR)-21-3p and its predicted target FOXO3a in lung cancer cells was detected via reverse transcription-quantitative PCR, in the presence or absence of nicotine. The regulatory effect of miR-21-3p and FOXO3a on lung cancer cell proliferation and apoptosis induced by docetaxel or cisplatin treatment was evaluated by performing Cell Counting Kit-8 and Annexin V/PI staining assays, respectively. The interaction between miR-21-3p and FOXO3a was analyzed by performing luciferase reporter assays and western blotting. FOXO3a overexpression rescue experiments were conducted in vitro and in vivo using a xenograft mouse model to assess the function of miR-21-3p/FOXO3a in lung cancer. Nicotine induced miR-21-3p expression in lung cancer cells in a dose-dependent manner. miR-21-3p downregulated FOXO3a expression by directly binding to the 3′-untranslated region of FOXO3a. Moreover, miR-21-3p knockdown sensitized lung cancer cells to docetaxel or cisplatin treatment. Mechanistically, FOXO3a was predicted as a direct target of miR-21-3p. FOXO3a overexpression promoted the chemosensitivity of lung cancer cells to docetaxel or cisplatin treatment. Furthermore, FOXO3a overexpression antagonized the regulatory function of miR-21-3p on docetaxel- or cisplatin-treated lung cancer cells. In the docetaxel- or cisplatin-treated lung cancer xenograft mouse model, miR-21-3p promoted chemoresistance via negatively regulating FOXO3a. Therefore, the present study demonstrated that nicotine-induced miR-21-3p promoted chemoresistance to docetaxel or cisplatin treatment via negatively regulating FOXO3a, which may serve as a novel therapeutic strategy for the treatment of patients with chemoresistant lung cancer.

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Section: Discussionmentioning

confidence: 99%

Nicotine‑induced miR‑21‑3p promotes chemoresistance in lung cancer by negatively regulating FOXO3a

et al. 2022

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“…Currently, a variety of techniques are applied in lung cancer diagnosis including computed tomography (CT) scanning, fluorescence bronchoscopy, and polymerase chain reaction (PCR)‐based assay of the sputum (Andolfi, Potenza, et al, 2016; Field, Oudkerk, Pedersen, & Duffy, 2013; X. Li, Shen, & Luo, 2017; Pastorino, 2006; Shaw, Akufo‐Tetteh, Risk, Field, & Liloglou, 2006; Sutedja, Venmans, Smit, & Postmus, 2001). Chemotherapeutic agents such as paclitaxel (PTX; M. Zhang et al, 2020), docetaxel (DTX; N. Li, Mai, Liu, Gou, & Yang, 2020), cisplatin (CP; H. Zhu, Yang, & Yang, 2020), and gemcitabine (W. Cao et al, 2020) are used in lung cancer therapy. However, the resistance of lung cancer cells has significantly diminished the efficacy of chemotherapeutic agents in the eradication of lung cancer.…”

Section: Lung Cancer: Epidemiology and Treatmentmentioning

confidence: 99%

“…Noteworthy, there are endogenous inhibitors that negatively affect STAT3 expression to suppress its activity. Suppressor of cytokine signaling 1 and 3 (SOCS1 and SOCS3) are STAT3 inhibitors and their downregulation elevates the proliferation of cancer cells (N. Li et al, 2020; K. J. Zhang, Tan, & Guo, 2020). Curcumin is capable of enhancing the expression of SOCS3 and SOCS1 to inhibit STAT3 and lung cancer growth (Tang et al, 2018).…”

Section: Curcumin and Lung Cancermentioning

confidence: 99%

Versatile role of curcumin and its derivatives in lung cancer therapy

Ashrafizadeh

Najafi

Makvandi

et al. 2020

Journal Cellular Physiology

104

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Lung cancer is a main cause of death all over the world with a high incidence rate. Metastasis into neighboring and distant tissues as well as resistance of cancer cells to chemotherapy demand novel strategies in lung cancer therapy. Curcumin is a naturally occurring nutraceutical compound derived from Curcuma longa (turmeric) that has great pharmacological effects, such as anti‐inflammatory, neuroprotective, and antidiabetic. The excellent antitumor activity of curcumin has led to its extensive application in the treatment of various cancers. In the present review, we describe the antitumor activity of curcumin against lung cancer. Curcumin affects different molecular pathways such as vascular endothelial growth factors, nuclear factor‐κB (NF‐κB), mammalian target of rapamycin, PI3/Akt, microRNAs, and long noncoding RNAs in treatment of lung cancer. Curcumin also can induce autophagy, apoptosis, and cell cycle arrest to reduce the viability and proliferation of lung cancer cells. Notably, curcumin supplementation sensitizes cancer cells to chemotherapy and enhances chemotherapy‐mediated apoptosis. Curcumin can elevate the efficacy of radiotherapy in lung cancer therapy by targeting various signaling pathways, such as epidermal growth factor receptor and NF‐κB. Curcumin‐loaded nanocarriers enhance the bioavailability, cellular uptake, and antitumor activity of curcumin. The aforementioned effects are comprehensively discussed in the current review to further direct studies for applying curcumin in lung cancer therapy.

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“…Other compounds that can be used to reduce the drug pumping in the liposome-based carriers out are coumarin, TGPS, or hydroxypropyl-β-cyclodextrin (HP-β-CD). In a study by Li et al [ 79 ] , liposomes were co-loaded with coumarin and DOX and coated with TGPS, and their efficiency was tested against resistant A549/DDP cells, both in vitro and in vivo , as a xenograft tumor in the mice model. The materials were found to be readily up-taken by cancer cells, reducing their viability by up to 90%.…”

Section: Nanocarriers For the Treatment Of Drug Resistance In Tumorsmentioning

confidence: 99%

Nanocarrier drug resistant tumor interactions: novel approaches to fight drug resistance in cancer

Benko¹

2020

CDR

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Cancer is one of the biggest healthcare concerns in our century, a disease whose treatment has become even more difficult following reports of drug-resistant tumors. When this happens, chemotherapy treatments fail or decrease in efficiency, leading to catastrophic consequences to the patient. This discovery, along with the fact that drug resistance limits the efficacy of current treatments, has led to a new wave of discovery for new methods of treatment. The use of nanomedicine has been widely studied in current years as a way to effectively fight drug resistance in cancer. Research in the area of cancer nanotechnology over the past decades has led to tremendous advancement in the synthesis of tailored nanoparticles with targeting ligands that can successfully attach to chemotherapy-resistant cancer by preferentially accumulating within the tumor region through means of active and passive targeting. Consequently, these approaches can reduce the off-target accumulation of their payload and lead to reduced cytotoxicity and better targeting. This review explores some categories of nanocarriers that have been used in the treatment of drug-resistant cancers, including polymeric, viral, lipid-based, metal-based, carbon-based, and magnetic nanocarriers, opening the door for an exciting field of discovery that holds tremendous promise in the treatment of these tumors.

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Docetaxel-loaded D-α-tocopheryl polyethylene glycol-1000 succinate liposomes improve lung cancer chemotherapy and reverse multidrug resistance

Cited by 33 publications

References 47 publications

Nicotine‑induced miR‑21‑3p promotes chemoresistance in lung cancer by negatively regulating FOXO3a

Nicotine‑induced miR‑21‑3p promotes chemoresistance in lung cancer by negatively regulating FOXO3a

Versatile role of curcumin and its derivatives in lung cancer therapy

Nanocarrier drug resistant tumor interactions: novel approaches to fight drug resistance in cancer

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