Molecular approaches for targeted drug delivery towards cancer: A concise review with respect to nanotechnology

被引:39
作者
Das Kurmi, Balak [1 ]
Patel, Preeti [1 ]
Paliwal, Rishi [2 ]
Paliwal, Shivani Rai [1 ]
机构
[1] Guru Ghasidas Vishwavidyalaya, SLT Inst Pharmaceut Sci, Bilaspur, CG, India
[2] Indira Gandhi Natl Tribal Univ, Dept Pharm, Nanomed & Bioengn Res Lab, Amarkantak, MP, India
关键词
NF-KAPPA-B; NANOPARTICLES INDUCE APOPTOSIS; TUMOR-ASSOCIATED MACROPHAGES; SELECTIVE BCL-2 INHIBITOR; RECEPTOR TYROSINE KINASES; HUMAN MONOCLONAL-ANTIBODY; TRAIL-INDUCED APOPTOSIS; BREAST-CANCER; GROWTH-FACTOR; ANTITUMOR-ACTIVITY;
D O I
10.1016/j.jddst.2020.101682
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cancer is a leading cause of human death throughout the world. The lack of specificity associated with conventional anti-cancer therapeutics leads to several side effects in addition. Cancer initiation and progression involve complex and multi carcinogenesis processes along with diverse cellular physiological system activities like cell signaling and apoptosis. An erratic microenvironment and drug resistance mechanism of cancer cells further causes failure of the most conventional chemotherapy regimen. Such limitations of the conventional cancer therapy advocate well engineered and smart therapeutics for cancer treatment. An ideal cancer treatment needs a customized and specialized drug delivery technology, which is capable to eradicate even a last cancer cell that may be responsible for the relapse of disease. Targeted nanocarriers (NCs) navigate the loaded therapeutics towards the specific site of action with the reduced adverse effects on the healthy cells. This review presents an overview of various molecular mechanisms and cellular alterations associated with cancer cell development and how targeted formulations can be designed for cancer therapy. A brief focuses on the applications of nanotechnology to exploit these mechanisms and molecular ports for the development of a novel targeted formulation for cancer treatment has also been discussed. © 2020 Elsevier B.V.
引用
收藏
页数:22
相关论文
共 333 条
[61]   EGFR aptamer-conjugated liposome-polycation-DNA complex for targeted delivery of SATB1 small interfering RNA to choriocarcinoma cells [J].
Dong, Jinhua ;
Cao, Yunfei ;
Shen, Huaxiang ;
Ma, Qiang ;
Mao, Shuhui ;
Li, Suping ;
Sun, Jin .
BIOMEDICINE & PHARMACOTHERAPY, 2018, 107 :849-859
[62]   Mechanisms of receptor tyrosine kinase activation in cancer [J].
Du, Zhenfang ;
Lovly, Christine M. .
MOLECULAR CANCER, 2018, 17
[63]   FK506, an immunosuppressant targeting calcineurin function [J].
Dumont, FJ .
CURRENT MEDICINAL CHEMISTRY, 2000, 7 (07) :731-748
[64]   Angiogenesis inhibitors in cancer therapy: mechanistic perspective on classification and treatment rationales [J].
El-Kenawi, Asmaa E. ;
El-Remessy, Azza B. .
BRITISH JOURNAL OF PHARMACOLOGY, 2013, 170 (04) :712-729
[65]   Carbon Nanotubes in Cancer Therapy and Drug Delivery [J].
Elhissi, Abdelbary M. A. ;
Ahmed, Waqar ;
Hassan, Israr Ul ;
Dhanak, Vinod. R. ;
D'Emanuele, Antony .
JOURNAL OF DRUG DELIVERY, 2012, 2012
[66]   VEGF-targeted therapy: mechanisms of anti-tumour activity [J].
Ellis, Lee M. ;
Hicklin, Daniel J. .
NATURE REVIEWS CANCER, 2008, 8 (08) :579-591
[67]   Modulation of nuclear factor-kappa B activation by the endoplasmic reticulum stress sensor PERK to mediate estrogen- induced apoptosis in breast cancer cells [J].
Fan, Ping ;
Tyagi, Amit K. ;
Agboke, Fadeke A. ;
Mathur, Rohit ;
Pokharel, Niranjana ;
Jordan, V. Craig .
CELL DEATH DISCOVERY, 2018, 4
[68]   Angiogenesis as a therapeutic target [J].
Ferrara, N ;
Kerbel, RS .
NATURE, 2005, 438 (7070) :967-974
[69]   Cancer nanotechnology: Opportunities and challenges [J].
Ferrari, M .
NATURE REVIEWS CANCER, 2005, 5 (03) :161-171
[70]   ERADICATION OF SPONTANEOUS METASTASES AND ACTIVATION OF ALVEOLAR MACROPHAGES BY INTRAVENOUS-INJECTION OF LIPOSOMES CONTAINING MURAMYL DIPEPTIDE [J].
FIDLER, IJ ;
SONE, S ;
FOGLER, WE ;
BARNES, ZL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1981, 78 (03) :1680-1684