UNDERSTANDING OF PROTEIN-LIGAND INTERACTION FOR BREAST AND LUNG CANCER COMPOUNDS USING DOCKING...

www.wjpps.com Vol 4, Issue 1, 2015.

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Panduranga et al. World Journal of Pharmacy and Pharmaceutical Sciences

UNDERSTANDING OF PROTEIN-LIGAND INTERACTION FOR

BREAST AND LUNG CANCER COMPOUNDS USING

DOCKING METHOD

T. Panduranga Vital*1, G.S.V. Prasada Raju

2, D.S.V.G.K. Kaladhar

3

1CSE, Raghu Engineering College, Visakhapatnam, India.

2Dept. of Computer Science, School of Distance Education,Andhra University,

Visakhapatnam, India.

3Dept. of Microbiology and Bioinformatics, Bilaspur University, Bilaspur, India.

ABSTRACT

Proteins are structural and fundamental components which are directly

or indirectly related with the functioning of an organism. There are

more number of breast and lung cancers patients that are predicted in

the previous literature. The ATM (ataxia telangiectasia mutated) and

CHEK2 (checkpoint kinase 2) have the strongest evidence of being

related to the risk of developing breast cancer. EGFR and BRAF have

the evidence of being related to the risk of developing breast cancer.

AKT1 and PIK3CA are linked to both breast and lung cancers. The

Docking studies with selected compounds like Carmofur, Fenretinide,

Crizotinib, Docetaxel, Flavipiridol, Gemcitabine, Bexarotene,

Floxuridine and Satraplatin has been conducted using iGEMDOCK. The docking results

provided good scope for Docetaxel compound as anticanNcer drug for both lung and breast

cancers.

KEYWORDS: Docking, lung and breast cancers.

INTRODUCTIONProteins are complex organic macromolecules made up of amino acids.

[1,2] They are the structural and fundamental components of all living cells including many

substances, such as enzymes, antibodies and structural elements, which are directly or

indirectly related with the functioning of an organism. The disease causing activity is also

due on certain mutated proteins within the living system. [3]

WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES

SJIF Impact Factor 2.786

Volume 4, Issue 1, 945-966. Research Article ISSN 2278 – 4357

Article Received on

17 Oct 2014,

Revised on 12 Nov 2014,

Accepted on 09 Dec 2014

Nov 2014

*Correspondence for

Author

T. Panduranga Vital

CSE, Raghu Engineering

College, Visakhapatnam,

India.


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Prediction of intermolecular complex formation between receptor and ligand is an important

process in drug designing. [4,5]

Most of the drugs using by the cancer patients are known but

the better activity of drugs for particular genotype has to be better understood. The present

study can provide the better drugs using by the cancer patients from collected data have been

analyzed.

Methodology

There is more number of breast and lung cancer patients that are predicted in the collected

data from Andhra Pradesh, India. The protein sequences are collected from NCBI web site

related to lung and breast cancers and are modeled using swissmodel server. The ligands are

collected from DrugBank and are docked with iGEMDOCK for understanding the available

drugs using insilico tool. As on 23-05-2014, the query “breast cancer” in NCBI search with

protein showed 61116 reports. The AR, ATM, BARD1, BRIP1, CHEK2, DIRAS3, ERBB2,

NBN, PALB2, RAD50, and RAD51 genes are associated with breast cancer [6]. The CDH1,

STK11, and TP53 have been found to increase the risk of developing breast cancer. Some

research suggests that inherited variants of the ATM, BRIP1, CHEK2, BARD1, NBN,

PALB2, RAD50, and RAD51 genes, as well as certain versions of the AR gene, may also be

associated with breast cancer risk. However not all studies have shown these connections.

Hence the AR (androgen receptor), ATM, BRCA1, BRCA2, BARD1, CDH1, CHEK2,

BRIP1, DIRAS3, ERBB2, NBN, PALB2, RAD50, RAD51, STK11, and TP53 genes are

associated with breast cancer. Of these genes, ATM (ataxia telangiectasia mutated) and

CHEK2 (checkpoint kinase 2) have the strongest evidence of being related to the risk of

developing breast cancer.

A protein sequence for “breast cancer ataxia telangiectasia mutated” shown 29 reports and

the most relevant protein with accession number AAB38310 was selected, retrieved and

submitted to molecular modeling server, Swissmodel. Similarly protein sequence for “breast

cancer Checkpoint kinase 2” with accession number O96017 was retrieved and submitted to

molecular modeling server, Swissmodel. The modeled structures was shown in Figure 1.

>gi|1185510|gb|AAB38310.1| ataxia-telangiectasia mutated [Homo sapiens]

MTLHEPANSSASQSTDLCDFSGDLDPAPNPPHFPSHVIKATFAYISNCHKTKLKSILEI

LSKSPDSYQKILLAICEQAAETNNVYK

KHRILKIYHLFVSLLLKDIKSGLGGAWAFVLRDVIYTLIHYINQRPSCIMDVSLRSFSL

CCDLLSQVCQTAVTYCKDALENHLHVI


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VGTLIPLVYEQVEVQKQVLDLLKYLVIDNKDNENLYITIKLLDPFPDHVVFKDLRITQ

QKIKYSRGPFSLLEEINHFLSVSVYDAL

PLTRLEGLKDLRRQLELHKDQMVDIMRASQDNPQDGIMVKLVVNLLQLSKMAINHT

GEKEVLEAVGSCLGEVGPIDFSTIAIQHSK

DASYTKALKLFEDKELQWTFIMLTYLNNTLVEDCVKVRSAAVTCLKNILATKTGHSF

WEIYKMTTDPMLAYLQPFRTSRKKFLEVP

RFDKENPFEGLDDINLWIPLSENHDIWIKTLTCAFLDSGGTKCEILQLLKPMCEVKTD

FCQTVLPYLIHDILLQDTNESWRNLLST

HVQGFFTSCLRHFSQTSRSTTPANLDSESEHFFRCCLDKKSQRTMLAVVDYMRRQKR

PSSGTIFNDAFWLDLNYLEVAKVAQSCAA

HFTALLYAEIYADKKSMDDQEKRSLAFEEGSQSTTISSLSEKSKEETGISLQDLLLEIY

RSIGEPDSLYGCGGGKMLQPITRLRTY

EHEAMWGKALVTYDLETAIPSSTRQAGIIQALQNLGLCHILSVYLKGLDYENKDWCP

ELEELHYQAAWRNMQWDHCTSVSKEVEGT

SYHESLYNALQSLRDREFSTFYESLKYARVKEVEEMCKRSLESVYSLYPTLSRLQAIG

ELESIGELFSRSVTHRQLSEVYIKWQKH

SQLLKDSDFSFQEPIMALRTVILEILMEKEMDNSQRECIKDILTKHLVELSILARTFKN

TQLPERAIFQIKQYNSVSCGVSEWQLE

EAQVFWAKKEQSLALSILKQMIKKLDASCAANNPSLKLTYTECLRVCGNWLAETCL

ENPAVIMQTYLEKAVEVAGNYDGESSDELR

NGKMKAFLSLARFSDTQYQRIENYMKSSEFENKQALLKRAKEEVGLLREHKIQTNR

YTVKVQRELELDELALRALKEDRKRFLCKA

VENYINCLLSGEEHDMWVFRLCSLWLENSGVSEVNGMMKRDGMKIPTYKFLPLMY

QLAARMGTKMMGGLGFHEVLNNLISRISMDH

PHHTLFIILALANANRDEFLTKPEVARRSRITKNVPKQSSQLDEDRTEAANRIICTIRSR

RPQMVRSVEALCDAYIILANLDATQW

KTQRKGINIPADQPITKLKNLEDVVVPTMEIKVDHTGEYGNLVTIQSFKAEFRLAGGV

NLPKIIDCVGSDGKERRQLVKGRDDLRQ

DAVMQQVFQMCNTLLQRNTETRKRKLTICTYKVVPLSQRSGVLEWCTGTVPIGEFL

VNNEDGAHKRYRPNDFSAFQCQKKMMEVQK

KSFEEKYEVFMDVCQNFQPVFRYFCMEKFLDPAIWFEKRLAYTRSVATSSIVGYILGL

GDRHVQNILINEQSAELVHIDLGVAFEQ

GKILPTPETVPFRLTRDIVDGMGITGVEGVFRRCCEKTMEVMRNSQETLLTIVEVLLY

DPLFDWTMNPLKALYLQQRPEDETELHP


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TLNADDQECKRNLSDIDQSFDKVAERVLMRLQEKLKGVEEGTVLSVGGQVNLLIQQ

AIDPKNLSRLFPGWKAWV

>gi|6685284|sp|O96017. 1|CHK2_HUMAN RecName: Full=Serine/threonine-protein kinase

Chk2;

AltName: Full=CHK2 checkpoint homolog; AltName: Full=Cds1 homolog; Short=Hucds1;

Short=hCds1; AltName: Full=Checkpoint kinase 2

MSRESDVEAQQSHGSSACSQPHGSVTQSQGSSSQSQGISSSSTSTMPNSSQSSHSSSGT

LSSLETVSTQELYSIPEDQEPEDQEPE

EPTPAPWARLWALQDGFANLECVNDNYWFGRDKSCEYCFDEPLLKRTDKYRTYSK

KHFRIFREVGPKNSYIAYIEDHSGNGTFVNT

ELVGKGKRRPLNNNSEIALSLSRNKVFVFFDLTVDDQSVYPKALRDEYIMSKTLGSG

ACGEVKLAFERKTCKKVAIKIISKRKFAI

GSAREADPALNVETEIEILKKLNHPCIIKIKNFFDAEDYYIVLELMEGGELFDKVVGN

KRLKEATCKLYFYQMLLAVQYLHENGII

HRDLKPENVLLSSQEEDCLIKITDFGHSKILGETSLMRTLCGTPTYLAPEVLVSVGTA

GYNRAVDCWSLGVILFICLSGYPPFSEH

RTQVSLKDQITSGKYNFIPEVWAEVSEKALDLVKKLLVVDPKARFTTEEALRHPWLQ

DEDMKRKFQDLLSEENESTALPQVLAQPS

TSRKRPREGEAEGAETTKRPAVCAAVL.

ATM CHK2

Figure 1: Modeled structures for Breast cancer.

Lung cancer is due to genes like AKT1, ALK, BRAF, EGFR, HER2, KRAS, MEK1, MET,

NRAS, PIK3CA, RET, and ROS1. The EGFR and BRAF have the strongest evidence of

being related to the risk of developing breast cancer. AKT1 and PIK3CA are linked to both

breast and lung cancers.


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>gi|2811086|sp|P00533.2|EGFR_HUMAN RecName: Full=Epidermal growth factor

receptor; AltName: Full=Proto-oncogene c-ErbB-1; AltName: Full=Receptor

tyrosine-protein kinase erbB-1; Flags: Precursor

MRPSGTAGAALLALLAALCPASRALEEKKVCQGTSNKLTQLGTFEDHFLSLQRMFN

NCEVVLGNLEITYV

QRNYDLSFLKTIQEVAGYVLIALNTVERIPLENLQIIRGNMYYENSYALAVLSNYDAN

KTGLKELPMRNL

QEILHGAVRFSNNPALCNVESIQWRDIVSSDFLSNMSMDFQNHLGSCQKCDPSCPNG

SCWGAGEENCQKL

TKIICAQQCSGRCRGKSPSDCCHNQCAAGCTGPRESDCLVCRKFRDEATCKDTCPPL

MLYNPTTYQMDVN

PEGKYSFGATCVKKCPRNYVVTDHGSCVRACGADSYEMEEDGVRKCKKCEGPCRK

VCNGIGIGEFKDSLS

INATNIKHFKNCTSISGDLHILPVAFRGDSFTHTPPLDPQELDILKTVKEITGFLLIQAW

PENRTDLHAF

ENLEIIRGRTKQHGQFSLAVVSLNITSLGLRSLKEISDGDVIISGNKNLCYANTINWKK

LFGTSGQKTKI

ISNRGENSCKATGQVCHALCSPEGCWGPEPRDCVSCRNVSRGRECVDKCNLLEGEPR

EFVENSECIQCHP

ECLPQAMNITCTGRGPDNCIQCAHYIDGPHCVKTCPAGVMGENNTLVWKYADAGH

VCHLCHPNCTYGCTG

PGLEGCPTNGPKIPSIATGMVGALLLLLVVALGIGLFMRRRHIVRKRTLRRLLQEREL

VEPLTPSGEAPN

QALLRILKETEFKKIKVLGSGAFGTVYKGLWIPEGEKVKIPVAIKELREATSPKANKEI

LDEAYVMASVD

NPHVCRLLGICLTSTVQLITQLMPFGCLLDYVREHKDNIGSQYLLNWCVQIAKGMNY

LEDRRLVHRDLAA

RNVLVKTPQHVKITDFGLAKLLGAEEKEYHAEGGKVPIKWMALESILHRIYTHQSDV

WSYGVTVWELMTF

GSKPYDGIPASEISSILEKGERLPQPPICTIDVYMIMVKCWMIDADSRPKFRELIIEFSK

MARDPQRYLV

IQGDERMHLPSPTDSNFYRALMDEEDMDDVVDADEYLIPQQGFFSSPSTSRTPLLSSL

SATSNNSTVACI

DRNGLQSCPIKEDSFLQRYSSDPTGALTEDSIDDTFLPVPEYINQSVPKRPAGSVQNPV


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YHNQPLNPAPS

RDPHYQDPHSTAVGNPEYLNTVQPTCVNSTFDSPAHWAQKGSHQISLDNPDYQQDF

FPKEAKPNGIFKGS

TAENAEYLRVAPQSSEFIGA

>gi|50403720|sp|P15056.4|BRAF_HUMAN RecName: Full=Serine/threonine-protein

kinase B-raf; AltName: Full=Proto-oncogene B-Raf; AltName: Full=p94; AltName:

Full=v-Raf murine sarcoma viral oncogene homolog B1

MAALSGGGGGGAEPGQALFNGDMEPEAGAGAGAAASSAADPAIPEEVWNIKQMIK

LTQEHIEALLDKFGG

EHNPPSIYLEAYEEYTSKLDALQQREQQLLESLGNGTDFSVSSSASMDTVTSSSSSSLS

VLPSSLSVFQN

PTDVARSNPKSPQKPIVRVFLPNKQRTVVPARCGVTVRDSLKKALMMRGLIPECCAV

YRIQDGEKKPIGW

DTDISWLTGEELHVEVLENVPLTTHNFVRKTFFTLAFCDFCRKLLFQGFRCQTCGYK

FHQRCSTEVPLMC

VNYDQLDLLFVSKFFEHHPIPQEEASLAETALTSGSSPSAPASDSIGPQILTSPSPSKSIPI

PQPFRPAD

EDHRNQFGQRDRSSSAPNVHINTIEPVNIDDLIRDQGFRGDGGSTTGLSATPPASLPGS

LTNVKALQKSP

GPQRERKSSSSSEDRNRMKTLGRRDSSDDWEIPDGQITVGQRIGSGSFGTVYKGKWH

GDVAVKMLNVTAP

TPQQLQAFKNEVGVLRKTRHVNILLFMGYSTKPQLAIVTQWCEGSSLYHHLHIIETKF

EMIKLIDIARQT

AQGMDYLHAKSIIHRDLKSNNIFLHEDLTVKIGDFGLATVKSRWSGSHQFEQLSGSIL

WMAPEVIRMQDK

NPYSFQSDVYAFGIVLYELMTGQLPYSNINNRDQIIFMVGRGYLSPDLSKVRSNCPKA

MKRLMAECLKKK

RDERPLFPQILASIELLARSLPKIHRSASEPSLNRAGFQTEDFSLYACASPKTPIQAGGY

GAFPVH

>gi|133777895|gb|AAI15584.1| Akt1 protein, partial [Mus musculus]

QIHEDSRDGHIKITDFGLCKEGIKDGATMKTFCGTPEYLAPEVLEDNDYGRAVDWW

GLGVVMYEMMCGRL

PFYNQDHEKLFELILMEEIRFPRTLGPEAKSLLSGLLKKDPTQRLGGGSEDAKEIMQH


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RFFANIVWQDVY

EKKLSPPFKPQVTSETDTRYFDEEFTAQMITITPPDQDDSMECVDSERRPHFPQFSYSA

SGTA

>gi|126302584|sp|P42336.2|PK3CA_HUMAN RecName: Full=Phosphatidylinositol 4,5-

bisphosphate 3-kinase catalytic subunit alpha isoform; Short=PI3-kinase

subunit alpha; Short=PI3K-alpha; Short=PI3Kalpha; Short=PtdIns-3-kinase

subunit alpha; AltName: Full=Phosphatidylinositol 4,5-bisphosphate 3-kinase

110 kDa catalytic subunit alpha; Short=PtdIns-3-kinase subunit p110-alpha;

Short=p110alpha; AltName: Full=Phosphoinositide-3-kinase catalytic alpha

polypeptide; AltName: Full=Serine/threonine protein kinase PIK3CA

MPPRPSSGELWGIHLMPPRILVECLLPNGMIVTLECLREATLITIKHELFKEARKYPLH

QLLQDESSYIF

VSVTQEAEREEFFDETRRLCDLRLFQPFLKVIEPVGNREEKILNREIGFAIGMPVCEFD

MVKDPEVQDFR

RNILNVCKEAVDLRDLNSPHSRAMYVYPPNVESSPELPKHIYNKLDKGQIIVVIWVIV

SPNNDKQKYTLK

INHDCVPEQVIAEAIRKKTRSMLLSSEQLKLCVLEYQGKYILKVCGCDEYFLEKYPLS

QYKYIRSCIMLG

RMPNLMLMAKESLYSQLPMDCFTMPSYSRRISTATPYMNGETSTKSLWVINSALRIK

ILCATYVNVNIRD

IDKIYVRTGIYHGGEPLCDNVNTQRVPCSNPRWNEWLNYDIYIPDLPRAARLCLSICS

VKGRKGAKEEHC

PLAWGNINLFDYTDTLVSGKMALNLWPVPHGLEDLLNPIGVTGSNPNKETPCLELEF

DWFSSVVKFPDMS

VIEEHANWSVSREAGFSYSHAGLSNRLARDNELRENDKEQLKAISTRDPLSEITEQEK

DFLWSHRHYCVT

IPEILPKLLLSVKWNSRDEVAQMYCLVKDWPPIKPEQAMELLDCNYPDPMVRGFAV

RCLEKYLTDDKLSQ

YLIQLVQVLKYEQYLDNLLVRFLLKKALTNQRIGHFFFWHLKSEMHNKTVSQRFGL

LLESYCRACGMYLK

HLNRQVEAMEKLINLTDILKQEKKDETQKVQMKFLVEQMRRPDFMDALQGFLSPLN

PAHQLGNLRLEECR

IMSSAKRPLWLNWENPDIMSELLFQNNEIIFKNGDDLRQDMLTLQIIRIMENIWQNQG


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LDLRMLPYGCLS

IGDCVGLIEVVRNSHTIMQIQCKGGLKGALQFNSHTLHQWLKDKNKGEIYDAAIDLF

TRSCAGYCVATFI

LGIGDRHNSNIMVKDDGQLFHIDFGHFLDHKKKKFGYKRERVPFVLTQDFLIVISKG

AQECTKTREFERF

QEMCYKAYLAIRQHANLFINLFSMMLGSGMPELQSFDDIAYIRKTLALDKTEQEALE

YFMKQMNDAHHGG

WTTKMDWIFHTIKQHALN

The modeled structures for above sequences are shown in was shown in Figure 2.

EGFR BRAF Akt1 PIK3CA

Figure 2: Modeled structures for lung cancer.

The drug molecules are retrieved based on the prescribed medical data. The 3D molecules of

the drugs have been retrieved from DrugBank. Table 1 was shown the prescribed drug with

DrugBank Identifier and target for cancer. The structures for the selected ligands are

presented in Figure 3.

Table 1: Drug with DrugBank Identifier and target for cancer.

Prescribed drug DrugBank ID Type of cancer

Carmofur DB09010 Breast

Fenretinide DB05076 Breast

Crizotinib DB08865 Lung

Docetaxel DB01248 Breast- Lung

Flavipiridol DB03496 Breast

Gemcitabine DB00441 Lung - Breast

Bexarotene DB00307 Lung - Breast

Floxuridine DB00322 Lung

Satraplatin DB04996 Lung


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Carmofur Fenretinide Crizotinib Docetaxel Flavipiridol

Gemcitabine Floxuridine Bexarotene Satraplatin

Figure 3: Ligand structures.

RESULTS AND DISCUSSION

The docking analysis was done using iGEMDOCK. The docked results for breast cancer

targeted drugs were presented in Table 2. In the prescribed drugs Docetaxel has good binding

affinity for ATM and CHK2 molecules (Breast cancer).

Table 2: Docking report for breast cancer molecules.

Compounds Binding energies in Kcal/mole

ATM CHK2

Carmofur -85.41 -83.9

Fenretinide -80.8 -83.7

Crizotinib -86.9 -82.14

Docetaxel -130.3 -114.16

Flavipiridol -108.8 -78.5

Gemcitabine -87.8 -82.2

Bexarotene -77.6 -72.1

Floxuridine -81.3 -83.2

Satraplatin -84.8 -69.8

Figures 4 and 5 were shown the docked poses for breast cancer causing proteins with selected

drugs.


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4 (A) Carmofur and ATM 4 (B) Fenretinide and ATM

4 (C) Crizotinib and ATM 4 (D) Docetaxel and ATM

4 (E) Flavipiridol and ATM 4 (F) Gemcitabine and ATM

4 (G) Bexarotene and ATM 4 (H) Floxuridine and ATM


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4 (I) Satraplatin and ATM

Figure 4: Ligand-Protein docking structures for breast cancer causing gene ATM.

5 (A) Carmofur and CHK2

5 (B) Fenretinide and CHK2 5 (C) Crizotinib and CHK2


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5 (D) Docetaxel and CHK2 5 (E) Flavipiridol and CHK2

5 (F) Gemcitabine and CHK2 5 (G) Bexarotene and CHK2

5 (H) Floxuridine and CHK2 5 (I) Satraplatin and CHK2

Figure 5: Ligand-Protein docking structures for breast cancer causing gene CHK2.


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Table 3: Docking report for lung cancer molecules.


EGFR BRAF

Carmofur -75.3 -87.6

Fenretinide -80.9 -85

Crizotinib -90.6 -100.1

Docetaxel -130.7 -136.9

Flavipiridol -93.4 -97

Gemcitabine -94.1 -88.2



Satraplatin -70 -77.5

The docking analysis for lung cancer with selected ligand was done using

iGEMDOCK Table 3 and Figures 6 and 7). In the prescribed drugs Docetaxel has good

binding affinity for EGFR and BRAF molecules (lung cancer).

6(A) Carmofur and EGFR 6(B) Fenretinide and EGFR

6(C) Crizotinib and EGFR 6(D) Docetaxel and EGFR


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6(E) Flavipiridol and EGFR 6(F) Gemcitabine and EGFR

6(G) Bexarotene and EGFR 6(H) Floxuridine and EGFR

6(I) Satraplatin and EGFR

Figure 6: Ligand-Protein docking structures for lung cancer causing gene EGFR.


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7(A) Carmofur and BRAF

7(B) Fenretinide and BRAF 7(C) Crizotinib and BRAF

7(D) Docetaxel and BRAF 7(E) Flavipiridol and BRAF


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7(F) Gemcitabine and BRAF 7(G) Bexarotene and BRAF

7(H) Floxuridine and BRAF 7(I) Satraplatin and BRAF

Figure 7: Ligand-Protein docking structures for lung cancer causing gene BRAF.

Table 4: Docking report for lung/ Breast cancer molecules.


AKT1 PIK3CA

Carmofur -87.8 -69.5

Fenretinide -79.8 -74.2

Crizotinib -90 -82.5

Docetaxel -115.2 -123.8

Flavipiridol -93.35 -77.9

Gemcitabine -81.9 -73



Satraplatin -69.6 -60.1

The docking analysis for lung and breast cancer causing proteins with selected ligand was

done using iGEMDOCK Table 4 and Figures 8 and 9). Docetaxel has good binding affinity


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for AKT1 and PIK3CA molecules (lung/ Breast cancers).

8(A) Carmofur and AKT1

8(B) Fenretinide and AKT1

8(C) Crizotinib and AKT1


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8(D) Docetaxel and AKT1

8(E) Flavipiridol and AKT1

8(F) Gemcitabine and AKT1


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8(G) Bexarotene and AKT1

8(H) Floxuridine and AKT1

8(I) Satraplatin and AKT1

Figure 8 Ligand-Protein docking structures for lung and breast cancer causing protein

AKT1.


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9(A) Carmofur and PIK3CA

9(B) Fenretinide and PIK3CA 9(C) Crizotinib and PIK3CA

9(D) Docetaxel and PIK3CA 9(E) Flavipiridol and PIK3CA


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9(F) Gemcitabine and PIK3CA 9(G) Bexarotene and PIK3CA

9(H) Floxuridine and PIK3CA 9(I) Satraplatin and PIK3CA

Figure 9: Ligand-Protein docking structures for lung and breast cancer causing protein

PIK3CA.

The docking results provided good scope for Docetaxel compound as anticancer drug for

both lung and breast cancers. Treatment with single-agent docetaxel was provided longer

survival and best supportive care in patients with non–small-cell lung cancer [7,8]. Treatment

with docetaxel is associated with significant prolongation of survival and the benefits of

docetaxel therapy outweigh the risks.

CONCLUSION

The docking reports shown that Docetaxel compound has better suppressor activity for both

lung and breast cancers.


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ACKNOWLEDGEMENTS

The authors thank to Bilaspur University, Bilaspur and GITAM University, Visakhapatnam

for providing technical facilities.

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