Dab tsi yog cov inhibitors zoo rau kev kho mob qog noj ntshav thiab fibrosis?---Part 2
Mar 03, 2022
Hu rau: emily.li@wecistanche.com
Me Molecule Inhibitors Ntawm Epithelial-mesenchymal Hloov Rau Kev Kho Mob Cancer Thiab Fibrosis
Ya Long Feng1| Dan-Qian Chen1| Nosratola D. Vaziri2| Yan Guo1,3 |Ying-Yong Zhao1
Abstract
Cov ntaub so ntswgfibrosis thiabmob qog noj ntshavob qho tib si ua rau muaj mob hnyav thiab tuag thoob ntiaj teb; yog li ntawd, cov tswv yim kho tau zoo yog qhov xav tau sai. Vim tias cov tshuaj tiv thaiv tau nthuav dav hauv cov ntaub so ntswg fibrotic thiabmob qog noj ntshav, tsim kom muaj lub tswv yim los nrhiav cov hom phiaj tshiab rau kev cuam tshuam cov tshuaj yog tsim nyog rau kev kho mob zoofibrosisthiabmob qog noj ntshav. Txawm tias muaj ntau yam ua raufibrosisthiabmob qog noj ntshav, pathophysiological tsom xam tau pom tias cov ntaub so ntswgfibrosisthiabmob qog noj ntshavqhia ib tug txheej txheem ntawmepithelial-mesenchymalKev hloov pauv (EMT). EMT cuam tshuam nrog ntau tus neeg nruab nrab, suav nrog cov xwm txheej hloov pauv (Snail, zinc-ntiv tes E-box-binding protein thiab teeb liab transducer thiab activator ntawm transcription 3), kev taw qhia txoj hauv kev (transform-ing growth factor-1, RAC-serine/threonine-protein kinase, Wnt, nuclear factor-kappa B, peroxisome proliferator-activated receptor, Notch, thiab RAS), RNA-binding proteins (ESRP1 thiab ESRP2) thiab microRNAs. Yog li, cov tshuaj tsom rau EMT tej zaum yuav yog ib qho kev cog lus kho mob rau ob leegfibrosisthiab qog. Ib tug loj tus naj npawb ntawm cov tebchaw uas yog synthesized los yog muab tau los ntawm tej yam ntuj tso khoom thiab lawv derivatives suppress EMT los ntawm lub hom phiaj ntawm cov neeg nruab nrab hauvfibrosisthiab mob qog noj ntshav. Los ntawm lub hom phiaj EMT, cov tebchaw no tau nthuav tawm cov teebmeem tshuaj tiv thaiv kabmob hauv ntau hom kabmob kheesxaws, thiab qee qhov ntawm lawv kuj pom cov teebmeem antifibrotic. Yog li ntawdCov tshuaj tsom EMT tsis tsuas yog muaj cov tshuaj tua kab mob thiabtshuaj tiv thaiv kab mobcov teebmeem tab sis kuj tseem siv tau cov teebmeem kev kho mob ntawm ntau lub cevfibrosis thiab mob cancer, uas muab kev kho mob zoo tiv thaivfibrosisthiabmob qog noj ntshav. Ua ke, cov txiaj ntsig tau hais qhia hauv qhov kev tshuaj xyuas no muab cov tswv yim tshiab rau kev tshawb pom cov tshuaj antifibrotic tshiab thiab tshuaj tua kab mob.
KEYWORDS:mob qog noj ntshav, epithelial-mesenchymalkev hloov pauv,fibrosis, natural khoom, me me molecule, transcription factor, qog
Ntu 2
Cistanche yog qhov zoo rau kev tiv thaiv kab mob qog noj ntshav thiab fibrosis
2.2.4|Akt signaling txoj kev
Akt (tseem hu ua protein kinase B lossis Rac) yog serine / threonine tshwj xeeb protein kinase uas ua lub luag haujlwm tseem ceeb hauv ntau yam kev ua ntawm tes. Ntau lub xov tooj ntawm tes tau hloov pauv los ntawm Akt signaling pathway, thiab Akt koom nrog EMT hauv kev koom tes nrog lwm cov proteins. Piv txwv li, tripartite motif-muaj 14 yog ib qho oncogene uas tswj EMT thiab metastasis ntawm tib neeg plab hnyuv cancer los ntawm activating Akt signaling.168 M3 muscarinic acetylcholine receptors tswj EMT, perineural ntxeem tau, thiab metastasis nyob rau hauv cholangiocarcinoma.1 homokt. txhawb EMT los ntawm kev ua kom lub Akt/GSK3 txoj hauv kev uas tsis yog-hlwb-hlwb-hlwb mob ntsws cancer.170 Akt signaling pathway mediated cigarette-induced EMT in lung cancer.171 Tsis tas li ntawd, Akt kuj txhawb EMT kev koom tes nrog miRNAs. MiR-944 inhibited EMT thiab metastasis ntawm gastric mob cancer los ntawm metastasis-txuas nrog txoj hnyuv loj 1 (MACC1) / Met/Akt signaling pathway.172 MiR-1296 inhibited EMT thiab metastasis ntawm hepatocellular carcinoma ntawm serine / threonine-1296 protein kinase. /PI3K/Akt signaling pathway.173Tau ua ke, cov ntaub ntawv no qhia tias Akt ua lub luag haujlwm tseem ceeb hauv EMT xov tooj ntawm tes hloov pauv thiab tias kev tsom mus rau Akt tej zaum yuav yog txoj hauv kev zoo rau kev kho mob.fibrosisthiabqog nqaij hlav(Table 1).
Simvastatin yog 3-hydroxy-3-methylglutaryl coenzyme A inhibitor uas yog siv los kho cov kab mob plawv. Tsis ntev los no, nws tau tshaj tawm tias simvastatin muaj kev kho mob hauv ntau yam qog nqaij hlav. Kev tswj hwm ntawm simvastatin suppressed EMT los ntawm phosphatase thiab tensin homolog (PTEN) / PI3K / Akt txoj hauv EC9706-Rcells, qhia txog kev kho mob tshiab rau simvastatin hauv cov qog nqaij hlav.34 Trichostatin A, histone deacetylase inhibitor, yog tshuaj tua kab mob. Ntxiv rau nws cov khoom siv tshuaj tua kab mob, trichostatin A alleviated EMT hauv bleomycin-induced ntsws raug mob hauv cov nas los ntawm inhibiting Akt signaling pathwayUbenimex inhibits ntau yam proteases, suav nrog arginyl aminopeptidase, leukotriene A4 hydrolase, alanyl aminopeptidase, thiab leuceptyl/cysteidasepidase, amino acids. kho mob myelocytic leukemia thiab lymphedema. Ubenimex alleviated tau txais sorafenib (ib kab tshuaj tiv thaiv kab mob thawj zaug) tsis kam nyob rau hauv lub raum cell carcinoma ntawm suppressing txoj kev Akt.
Luteolin yog dav faib nyob rau hauv cov nroj tsuag thiab tau qhia anti-inflammatory, antioxidant, antimicrobial, thiab antitumor zog. Luteolin attenuated TGF-1-induced EMT los ntawm kev kho cov PI3K/Akt/NF-κB-Snail txoj hauv kev mob ntsws cancer37 (Daim duab 2). Tsis tas li ntawd, luteolin txo qis kev mob qog noj ntshav los ntawm kev thim rov qab EMT ntawm txoj kev taw qhia kev taw qhia.38 Tsis tas li ntawd, luteolin kuj inhibited cov metastasis ntawm triple-negative mob cancer ntawm lub mis los ntawm kev thaiv EMT los ntawm downregulation ntawm -catenin.174 Tsis tas li ntawd, luteolin suppressed EMT los ntawm downregulating cov kev qhia ntawm cyclic AMP- teb cov ntsiab lus-binding protein 1175 nyob rau hauv colorectal cancer hlwb.176 Collectively, luteolin pom cov kev kho mob nyob rau hauv ob qho tib si cov ntaub so ntswg fibrosis thiab qog los ntawm ntau yam signaling pathways thiab tej zaum yuav yog ib tug pheej yig neeg sib tw raukho fibrosis thiab qog.
-Mangostin muab tau los ntawm pericarp ntawm mangosteen txiv hmab txiv ntoo tau pom tias muaj ntau yam cellular zog, xws li ntes lub voj voog ntawm tes, inhibiting cell viability, inducing apoptosis, thiab sib txawv, txo o, thiab txo adhesion. -Mangostin suppressed viability thiab EMT los ntawm downregulating PI3K / Akt txoj hauv kev mob qog noj ntshav pancreatic.89 Icaritin, cov khoom siv hydrolytic ntawm icariin uas cais tawm los ntawm cov tswv cuab ntawm epimedium genus, induced trans-differentiation ntawm embryonic qia hlwb rau hauv cardiomyocytes, tiv thaiv. txuam nrog osteonecrosis thiab stimulated neuronal sib txawv.36 Icaritin inhibited ntxeem tau thiab EMT ntawm lub hom phiaj PTEN / Akt / HIF-1 txoj kev taw qhia
2.2.5|PPAR signaling txoj kev
PPAR belongs rau cov tshuaj hormones receptor superfamily thiab muaj peb isoforms xws li PPAR, PPAR / δ, thiab PPAR. PPAR tau ua lub luag haujlwm tseem ceeb hauv kev tswj hwm ntawm cellular sib txawv, kev loj hlob, 12|FENG ET AL.metabolism, thiab tumorigenesis; tshwj xeeb, PPAR tau siv lub luag haujlwm tiv thaiv hauv kev txhim khofibrosisthiab qog. Ib txoj kev tshawb fawb tsis ntev los no tau qhia tias qhov ua kom ntawm PPAR attenuated cardiac fibrosis, uas tau kho los ntawm kev txo qis ntawm EMT thiab TGF- / ERK pathway.177 Ntxiv rau, qhov overexpression ntawm miR-130b txhawb EMT hauv glioma hlwb thiab tib neeg hepatocellular carcinoma, thiab PPAR tau raug txheeb xyuas tias yog lub hom phiaj ua haujlwm ntawm miR-130b, uas tau sib cuam tshuam nrog PPAR .178 Ntxiv mus, nws tau tshaj tawm tias PPAR agonist pioglitazone suppressed fibrotic kev hloov pauv hauv thawj cov liab retinal pigment epithelial hlwb los ntawm inhibiting TGF- signaling pathway.179 Sib sau ua ke. , cov txiaj ntsig no qhia tias PPAR yuav yog lub hom phiaj kho mobtiv thaiv fibrosis thiab qog(Table 1).
Evodiamine los ntawm Evodia rutaecarpa (Juss.) Benth. Cov tshuaj tiv thaiv kab mob, tiv thaiv kev rog, tiv thaiv kev ntxhov siab, tshuaj tiv thaiv kab mob, thiab tshuaj tiv thaiv kab mob. Evodiamine suppressed TGF-1-induced EMT hauv NRK-52E hlwb ntawm PPAR signaling pathway.53 Tsis tas li ntawd, curcumin yog ib qho tseem ceeb ntawm Curcuma longa L. uas nthuav tawm cov tshuaj tua kab mob, tshuaj tua kab mob, tshuaj tua kab mob, tshuaj tua kab mob, tshuaj tua kab mob, tshuaj tiv thaiv kab mob, thiab anticarcinogenic zog. Curcumin muaj cov nyhuv antifibrotic hauv plab hnyuv fibrosis thiab tiv thaiv EMT los ntawm PPAR txoj kev taw qhia.
2.2.6|Notch signaling txoj kev
Raws li kev txuag hluav taws xob zoo heev, lub Notch signaling txoj hauv kev tau koom nrog hauv kev loj hlob ntawm tes thiab kev sib txawv thaum lub sij hawm embryonic thiab cov neeg laus txoj kev loj hlob. Cov kev tshawb fawb dav dav tau pom tias txoj kev taw qhia kev taw qhia tseem ceeb heev rau EMT hauv cov qog nqaij hlav thiab fibrogenesis. Lub overexpression ntawm Notch1-induced EMT nyob rau hauv PC-3 hlwb, thiab claudin-1 pab EMT los ntawm lub Notch signaling txoj kev nyob rau hauv tib neeg bronchial epithelial hlwb.180,181 Tsis tas li ntawd, Notch thiab TGF-1 generated ib tug reciprocal zoo regulatory voj thiab kev koom tes tswj EMT. nyob rau hauv epithelial zes qe menyuam qog noj ntshav, uas muab kev pom tshiab rau hauv lub mechanism ntawm EMT.182Ntxiv mus, miR-34a downregulation induced los ntawm hypoxia enhanced EMT ntawm lub Notch signaling txoj kev nyob rau hauv tubular epithelial hlwb, uas qhia tau hais tias lub Notch signaling txoj kev tseem ceeb heev rau EMT thaum lub sij hawm fibrosis. .66 Cov xwm txheej no qhia tias qhov kev cuam tshuam rau lub hom phiaj ntawm txoj kev taw qhia kev taw qhia tej zaum yuav yog lub tswv yim zoo raukho mob cancer thiab fibrosis.
DAPT, ib-secretase inhibitor, txo qis kev qhia ntawm Snail thiab vimentin thiab nce E-cadherin qhia nyob rau hauv ob lub qhov ncauj squamous cell carcinoma cell kab, Tca8113 thiab CAL27, qhia tias lub hom phiaj inhibition ntawm Notch signaling txoj kev yuav yog ib tug tshiab kho tswv yim rau khomob qog noj ntshav.183,184 Lwm -secretase inhibitor, RO4929097, tsis tsuas yog inhibited EMT, ntxeem tau, thiab metastasis hauv ncauj tsev menyuam.mob qog noj ntshavHeLa thiab CaSki hlwb tab sis kuj tau siv cov kev kho mob tseem ceeb hauv cov neeg mob uas rov muaj mob glioma, ncauj tsev menyuam thiab hnyuv.mob qog noj ntshav, thiab cov qog nqaij hlav loj heev hauv kev sim tshuaj.67,185,186 3,6-Dihydroxyflavone yog ubiquitous nyob rau hauv zaub thiab txiv hmab txiv ntoo thiab blocksEMT nyob rau hauv lub mis mob hlwb los ntawm suppressing lub Notch signaling pathway.47 Ntxiv mus, luteolin inhibited EMT nyob rau hauv gastric cancer los ntawm lub Notch signaling pathway.38 Tsis tas li ntawd, emodin yog ib qho tseem ceeb bioactive tivthaiv ntawm Polygonumcuspidatum uas suppressed EMT nyob rau hauv alveolar epithelial hlwb ntawm lub Notch signaling txoj kev. Yog li ntawd, nws yog ib qho kev cia siab nyob rau hauv kev kho mob pulmonary fibrosis.96 Tsis tas li ntawd, berberine raug cais tawm ntawm Berberis vulgaris thiab thim rov qab EMT los ntawm kev thaiv cov Notch/Snail signaling pathway in nas with diabetes nephropathy.
2.2.7|RAS signaling pathway
RAS txoj kev taw qhia tsis yog tsuas yog tswj cov ntshav siab thiab cov kua dej sib npaug, tab sis kuj tseem koom nrog ntau yam kab mob, suav nrogmob qog noj ntshavthiabfibrosis. Tsis ntev los no, cov pov thawj tshwm sim tau qhia tias RAS kev taw qhia txoj hauv kev ua lub luag haujlwm tseem ceeb hauv EMT thaum lub sijhawmfibrosisthiab tumorigenesis. Angiotensin II txhawb EMT los ntawm kev sib cuam tshuam ntawm hematopoietic qia hlwb thiab stromal cell-derived factor-1/CXR4 axis hauv intrahepatic cholangiocarcinoma.187 Tsis tas li ntawd, qhov overexpression ntawm angiotensin II hom 1 receptor-induced EMT thiab txhawb cov qog nqaij hlav hauv tib neeg.mob qog noj ntshavcov hlwb, thiab kev ntsiag to ntawm angiotensin II hom 1 receptor suppressed EMT uas yog induced los ntawm cov piam thaj siab los ntawm inactivating mTOR/p70s6k signaling txoj kev nyob rau hauv tib neeg proximal tubular epithelial HK-2FENG ET AL.|13cell line.188,189 Raws li cov txiaj ntsig no, nws tau pom tias kev txo qis RAS yuav yog ib qho kev kho mob zoo los kho mob qog noj ntshav thiabfibrosis. Losartan yog AT1R antagonist uas txhim kho lub raumfibrosislos ntawm suppressing EMT hauv nas nrog hyperglycemia. 68Txawm hais tias ntau tus RAS inhibitors tau pom muaj txiaj ntsig zoo hauv cov qog thiab fibrosis, ob peb tau tshaj tawm tias inhibit EMT hauvkho mob cancer thiab fibrosis.
2.3|Targeting miRNA signaling pathways los ntawm me me molecules
MiRNAs yog endogenous me me uas tsis yog-coding RNAs (19-25 nucleotides) uas khi thaj tsam 3′-tsis tau txhais lus ntawm tus tub txib RNAs los tswj cov noob qhia. Tsis ntev los no, ntau miRNAs tau pom los txhawb lossis txwv EMTinfibrosisthiab qog. Piv txwv li, miRNA-497/Wnt3a/c-Jun tswj kev loj hlob thiab EMT, thiab miR-497 tau txais kev pab raws li ib tug qog suppressor nyob rau hauv glioma cells.192 Ntxiv mus, miR-205 inhibited qog loj hlob, ntxeem tau, thiab EMT ntawm lub hom phiaj semaphorin 4C nyob rau hauv hepatocellular. carcinoma.193 Tsis tas li ntawd, kev txhim kho ntawm miR-183-5p induced apoptosis thiab inhibited EMT, proliferation, ntxeem tau, thiab tsiv teb tsaws los ntawm downregulation ntawm ezrin nyob rau hauv tib neeg endometrialmob qog noj ntshavCell.194 Sib sau ua ke, EMT yog inhibited los ntawm ntau miRNAs, suav nrog miR-145, miR-497, miR-145-5p, miR-138, miR-200a, miR-200b, miR-655, miR-30-5p, thiab miR-32.
Cov flavonoids rhamnetin los ntawm cloves, berries, thiab cirsiliol los ntawm Cirsium lineare (Thunb.)Sch.—ib. pom muaj anti-inflammatory thiab antitumor zog. Ob leeg rhamnetin thiab cirsiliol induced xov tooj cua-sensitization thiab inhibited EMT los ntawm miR-34a / Notch1 signaling nyob rau hauv uas tsis yog-me-cell ntsws ntswsmob qog noj ntshavcells.40 Quercetin alleviated TGF-1-induced fibrosis nyob rau hauv HK-2 hlwb los ntawm downregulating miR-21 qhia thiab upregulating PTEN thiab TIMP metallopeptidase inhibitor 3 (TIMP3) expression.45 Sophocarpine los ntawm Sophora alopecuroides L. inhibited qog hlav thiab thim rov qab EMT. miR-21 nyob rau hauv lub taub hau thiab caj dabmob qog noj ntshav.51 Tsis tas li ntawd, sophocarpine tau ua kom muaj txiaj ntsig zoo los ntawm inhibiting EMT induced los ntawm TGF- .52 Zerumbone los ntawm Zingiber zerumbet (L.) Smith tau nthuav tawm.anti-inflammatorythiabmob qog noj ntshavkhoom. Tsis ntev los no, nws tau tshaj tawm tias cov pob txha zerum inhibited txoj kev-catenin ntawm miR-200c los thaiv EMT thiabmob qog noj ntshavstem cells.26 Ntxiv rau, nicotine upregulated FGFR3 thiab RB1 thiab txhawb EMT los ntawm downregulation ntawm miR-99b thiab miR-192 nyob rau hauv non-small-cell ntsws cancer hlwb.50Tsis tas li ntawd, ostiole alleviated EMT-mediated metastasis los ntawm inhibiting miR-23a-3p. .93 Tsis tas li ntawd, resveratrol inhibited proliferation, ntxeem tau, thiab EMT los ntawm upregulation ntawm miR-200c nyob rau hauv HCT-116 mob qog nqaij hlav hauv plab.
2.4|Targeting RNA splicing protein signaling txoj kev los ntawm me me molecules
RNA-binding proteins xws li RNA-binding Fox protein 2 (Rbfox2), epithelial splicing regulatory protein 1 (ESRP1), thiab ESRP2 tswj cov splicing ntawm ntau cov noob transcripts thiab splice nascent RNAs rau functionally thiab structurally sib txawv miRNAs tswj cov txheej txheem ntawm EMT. . Piv txwv li, bleomycin inhibited ESRP1 qhia, ua rau muaj kev sib txuas ntxiv ntawm FGFR2 rau nws cov mesenchymal isoform IIIc, uas ua rau EMT hauv lub ntsws.fibrosis.205 Tsis tas li ntawd, overexpressed ESRP1 pab txhawb EMT hauv zes qe menyuammob qog noj ntshav, inducing a cell-specific variant of CD44and a protein-enabled homolog.206 Ntxiv mus, Rbfox2 tau upregulated thaum lub sij hawm EMT, thiab lub depletion ntawm Rbfox2 suppressed qhov kev qhia ntawm mesenchymal marker noob.
Ntau qhov kev tshawb fawb tau qhia tias me me molecules tswj kev qhia ntawm RNA-binding proteins los kho EMT. Piv txwv li, caffeine, alkaloid nyob rau hauv tshuaj yej thiab kas fes, txo p53 qhia thiab upregulated p53 qhia los ntawm altering cov kev qhia ntawm serine/arginine-nplua nuj splicing factor 3 los tswj EMT.
2.5|Lwm yam tshiab mediators
Ntawm no, peb nthuav qhia qee tus neeg kho mob tshiab uas pab txhawb rau EMT nrog kev cia siab ntawm kev khofibrosisthiab qog. N-acetylglucosaminyltransferase, koom nrog tsev neeg ntawm glycosyltransferases, ua lub luag haujlwm tseem ceeb hauv EMT. Poob 14|FENG ET AL.N-acetylglucosaminyltransferase I induced cell-cell adhesion, txo cell migration, thiab suppressed cov lus qhia ntawm -SMA, vimentin, thiab N-cadherin, qhia txog inhibition ntawm EMT.208 Ntxiv mus, N-acetylgluco-aminotransferase MT I alleviated induced los ntawm TGF-1 hauv tib neeg MCF-10A hlwb.
Protein arginine methyltransferase 1 (PRMT1) mediates ntau yam tseem ceeb ntawm tes thiab ua lub luag haujlwm tseem ceeb hauvmob qog noj ntshavcell proliferation. Cov kev tshawb fawb tsis ntev los no tau qhia tias PRMT1 yog tus neeg kho mob tshiab ntawm EMT,mob qog noj ntshavcell migration, thiab ntxeem tau. Twist1 thiab E-cadherin yog lawv cov substrates.210 Cov kev tshawb pom no qhia tau hais tias kev tsom mus rau PRMT1-mediated Twist methylation tej zaum yuav yog lub tswv yim kho tshiab los kho.fibrosisthiab qog.
Histone H2A hom 2-c (Hist2h2ac) tau qhia hauv txhua lub mismob qog noj ntshav, thiab nws cov lus qhia tau raug ntxias los ntawm EGF hauv CD24 ntxiv / CD29hi / DC44hi cell subpopulation. Hist2h2ac silencing inhibited EGF-induced ZEB1 qhia thiab E-cadherin downregulation, uas qhia tias Hist2h2ac yog ib tug tshiab regulator ntawm EMT nyob rau hauv lub mis.mob qog noj ntshav.
EGF-zoo li rov ua dua thiab discoidin I-like domain-muaj protein ntau 3 (EDIL3) induced EMT thiab txhawb hepatocellular carcinoma migration, ntxeem tau, thiab angiogenesis nyob rau hauv vitro.212 Tsis tas li ntawd, lub overexpression ntawm EDIL3 induced lub activation ntawm ERK thiab TGF-kev taw qhia, tshem tawm ntawm EDIL3 suppressed EMT nyob rau hauv lub lens epithelial hlwb los ntawm TGF- signaling pathway.213 Tsis tas li ntawd, lub cytoplasmic qhia ntawm interleukin-zoo li EMT inducer (ILEI) yog ib tug muaj peev xwm marker ntawm EMT thiab qog kev loj hlob nyob rau hauv cov hnyuv.mob qog noj ntshav, thiab overexpression ntawm ILEI induced downregulation ntawm E-cadherin thiab upregulation ntawm vimentin.214 Txawm hais tias lub peev xwm ntawm cov tshiab mediators nyob rau hauv inducing ntaub so ntswg.fibrosisthiab cov qog tau raug tshawb xyuas, tsis muaj kev tshawb fawb tau tshaj tawm cov tshuaj tiv thaiv kab mob no tiv thaiv fibrosis thiab qog. Ua ke, cov txiaj ntsig no qhia tias cov neeg kho tshiab tshiab no ua lub luag haujlwm tseem ceeb hauv EMT, uas yuav muab lub hom phiaj tshiab rau cov khoom me me hauv kev tshawb fawb antifibrosis thiab antitumor yav tom ntej.
3|NYEEM NTXIV
Ob daim ntaubfibrosisthiab cov qog ua rau muaj mob hnyav thiab tuag thoob ntiaj teb; yog li ntawd, cov tswv yim kho tau zoo yog qhov xav tau sai. Kev tshawb nrhiav Mounting tau pom tias EMT ua lub luag haujlwm tseem ceeb hauvfibrosisthiab qog nqaij hlav, qhia tias cov tshuaj tsom rau EMT tej zaum yuav yog ib qho kev kho mob zoo tiv thaiv kab mob fibrosis thiab qog. Txawm hais tias TGF-1 yog ib qho muaj zog inducer ntawm EMT, lub hom phiaj tshiab yog xav tau vim yog lub luag haujlwm tsis sib haum xeeb ntawm TGF-1, uas tau pom tias muaj ntau lub luag haujlwm muaj txiaj ntsig hauv ntau yam bioactivities. Raws li cov ntsiab lus saum toj no, ntau tus neeg nruab nrab, suav nrog ntau yam kev hloov pauv (Snail, ZEB, thiab STAT3), kev taw qhia txoj hauv kev (NF-κB, Wnt, Akt, thiab PPAR), RNA-binding proteins (ESRP1 thiab ESRP2), thiab miRNAs, tswj EMT. . Kev tsom mus rau cov neeg kho kom haum xeeb no yuav yog ib qho kev kho tshiab rau kev kho mob antifibrosis thiab antitumor.
Ntau cov molecules me me suppress EMT los ntawm kev tsom mus rau cov neeg kho kom haum xeeb no, suav nrog cov tshuaj lag luam thiab cov khoom sib txuas tau los ntawm cov khoom ntuj. Tsis tas li ntawd, cov tebchaw uas lub hom phiaj EMT tau pom tias muaj kev tiv thaiv kabmob kheesxaws rau ntau hommob qog noj ntshav. Piv txwv li, luteolin tsis tsuas yog txo qis hauv plabmob qog noj ntshavtab sis kuj tau qhia txog kev kho mob hauv cov qog nqaij hlav ntsws. Yog li ntawd, peb xaus lus tias cov tebchaw tsom rau EMT ua rau muaj kev tiv thaiv kabmob kheesxaws hauv ib hom kabmob kheesxaws tuaj yeem siv tau rau lwm hom kabmob kheesxaws. Ntxiv mus, curcumin tsom EMT thiab nthuav tawm ob qho tib si anticancer thiab antifibrotic zog, uas qhia tias cov tshuaj tsom EMT tuaj yeem nthuav tawm ob qho tib si antifibrotic thiab anticancer. Ua ke, cov ntaub ntawv no qhia tias cov tshuaj tsom EMT tsis tsuas yog muaj cov tshuaj tiv thaiv kab mob thiab tshuaj tiv thaiv kab mob xwb tab sis kuj tseem muaj zog tiv thaiv ntau hom kabmob.fibrosisthiab mob qog noj ntshav, uas tuaj yeem pab tshawb nrhiav cov tshuaj kho mob tiv thaiv fibrosis thiab mob qog noj ntshav.
Cov molecules me me yog cov peev txheej loj rau bioactive ua cov tebchaw, thiab nws yog ib qho tseem ceeb kom nrhiav tau cov tshuaj bioactive tshiab kom zoo thiab sai. Ntawm no, peb tau sau ntau txoj hauv kev los tshawb xyuas qhov kev cia siab ntawm cov khoom ntuj tsim los ua cov neeg sib tw tshuaj. Ua ntej, molecular docking yog siv los kwv yees kev sib cuam tshuam ntawm ligand thiab lub hom phiaj protein, thiab molecular docking-raws li kev tshuaj ntsuam virtual yog pab tau rau kev ntxub ntxaug ntawm cov khoom sib txuas los ntawm cov tsis muaj zog. Tsis tas li ntawd, thaum lub sij hawm ua kom zoo dua cov hmoov txhuas, cov kev suav tuaj yeem sim hloov kho sai sai rau cov qauv ntawm cov khoom sib txuas uas paub txog ua ntej kev sib txuas. Yog li ntawd, cov txheej txheem suav nrog tuaj yeem ua kom nrawm qhov kev tshawb pom ntawm bioactive compounds. Thib ob, rov qab tshuaj pharmacokinetics yog siv rau kev tshawb nrhiav tshuaj los ntawm cov khoom ntuj tsim nrog FENG ET AL.|15 teev cov txiaj ntsig kho mob. Rov qab cov tshuaj pharmacokinetics tuaj yeem siv los coj cov ntaub so ntswg / cov kabmob / cov kabmob / molecules, thiab tom qab ntawd ntxiv cov qauv tshuaj uas cuam tshuam rau lub cev yog tsim los nrhiav cov tshuaj bioactive thiab qhia lawv cov txheej txheem sib xws.
Nws yog ib qho tsim nyog sau cia tias ntau lub tebchaw qhia tau tias tsis muaj kev solubility, uas txwv lawv cov kev kho mob thiab txwv tsis pub lawv siv tshuaj kho mob. Hmoov zoo, muaj ntau txoj hauv kev los txhim kho bioavailability, xws li cocrystallization thiab tsim cov phospholipid complexes thiab nanoemulsions.
Thaum kawg, raws li kev xav tias cov tshuaj tsom EMT muaj ob qho tib si tshuaj tiv thaiv kab mob thiab tshuaj tiv thaiv kab mob, ntau tus kws kho mob tseem ceeb pab txhawb rau EMT tau pom. Tsis tas li ntawd, ntau cov tshuaj tiv thaiv EMT hauv cov qog thiabfibrosislos ntawm kev tsom mus rau cov neeg kho kom haum xeeb no. Nws cia siab tias muaj ntau yam tshuaj tshiab tau tsim thiab tsim nyob rau yav tom ntej raws li cov kws kho mob tau hais tseg raukho cov qog thiab fibrosis.
TXOJ CAI
Txoj kev tshawb no tau txhawb nqa los ntawm National Natural Science Foundation ntawm Tuam Tshoj (Grant Nos. 81673578, 81872985,81603271).
Kev tsis sib haum xeeb ntawm kev txaus siab
Cov kws sau ntawv tshaj tawm tias tsis muaj qhov tsis sib haum xeeb ntawm kev txaus siab.
AUTHOR CONTRIBUTIONS
Txhua tus kws sau ntawv tau koom nrog hauv kev sau thiab kho cov ntawv sau no thiab tau muab kev pom zoo zaum kawg los xa.
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