RGD Reference Report - In situ analysis of mTORC1/2 and cellular metabolism-related proteins in human Lymphangioleiomyomatosis. - Rat Genome Database

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In situ analysis of mTORC1/2 and cellular metabolism-related proteins in human Lymphangioleiomyomatosis.

Authors: Krencz, Ildiko  Sebestyen, Anna  Papay, Judit  Jeney, Andras  Hujber, Zoltan  Burger, Charles D  Keller, Cesar A  Khoor, Andras 
Citation: Krencz I, etal., Hum Pathol. 2018 Sep;79:199-207. doi: 10.1016/j.humpath.2018.05.018. Epub 2018 Jun 6.
RGD ID: 152995523
Pubmed: PMID:29885404   (View Abstract at PubMed)
DOI: DOI:10.1016/j.humpath.2018.05.018   (Journal Full-text)

Lymphangioleiomyomatosis (LAM) is a rare progressive cystic lung disease with features of a low-grade neoplasm. It is primarily caused by mutations in TSC1 or TSC2 genes. Sirolimus, an inhibitor of mTOR complex 1 (mTORC1), slows down disease progression in some, but not all patients. Hitherto, other potential therapeutic targets such as mTOR complex 2 (mTORC2) and various metabolic pathways have not been investigated in human LAM tissues. The aim of this study was to assess activities of mTORC1, mTORC2 and various metabolic pathways in human LAM tissues through analysis of protein expression. Immunohistochemical analysis of p-S6 (mTORC1 downstream protein), Rictor (mTORC2 scaffold protein) as well as GLUT1, GAPDH, ATPB, GLS, MCT1, ACSS2 and CPT1A (metabolic pathway markers) were performed on lung tissue from 11 patients with sporadic LAM. Immunoreactivity was assessed in LAM cells with bronchial smooth muscle cells as controls. Expression of p-S6, Rictor, GAPDH, GLS, MCT1, ACSS2 and CPT1A was significantly higher in LAM cells than in bronchial smooth muscle cells (P<.01). No significant differences were found between LAM cells and normal bronchial smooth muscle cells in GLUT1 and ATPB expression. The results are uniquely derived from human tissue and indicate that, in addition to mTORC1, mTORC2 may also play an important role in the pathobiology of LAM. Furthermore, glutaminolysis, acetate utilization and fatty acid β-oxidation appear to be the preferred bioenergetic pathways in LAM cells. mTORC2 and these preferred bioenergetic pathways appear worthy of further study as they may represent possible therapeutic targets in the treatment of LAM.



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Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
ACSS2Humanlymphangioleiomyomatosis  IEP protein:increased expression:lung (human)RGD 
Acss2Ratlymphangioleiomyomatosis  ISOACSS2 (Homo sapiens)protein:increased expression:lung (human)RGD 
Acss2Mouselymphangioleiomyomatosis  ISOACSS2 (Homo sapiens)protein:increased expression:lung (human)RGD 
CPT1AHumanlymphangioleiomyomatosis  IEP protein:increased expression:lung (human)RGD 
Cpt1aRatlymphangioleiomyomatosis  ISOCPT1A (Homo sapiens)protein:increased expression:lung (human)RGD 
Cpt1aMouselymphangioleiomyomatosis  ISOCPT1A (Homo sapiens)protein:increased expression:lung (human)RGD 
GAPDHHumanlymphangioleiomyomatosis  IEP protein:increased expression:lung (human)RGD 
GLSHumanlymphangioleiomyomatosis  IEP protein:increased expression:lung (human)RGD 
GapdhRatlymphangioleiomyomatosis  ISOGAPDH (Homo sapiens)protein:increased expression:lung (human)RGD 
GapdhMouselymphangioleiomyomatosis  ISOGAPDH (Homo sapiens)protein:increased expression:lung (human)RGD 
GlsRatlymphangioleiomyomatosis  ISOGLS (Homo sapiens)protein:increased expression:lung (human)RGD 
GlsMouselymphangioleiomyomatosis  ISOGLS (Homo sapiens)protein:increased expression:lung (human)RGD 
RICTORHumanlymphangioleiomyomatosis  IEP protein:increased expression:lung (human)RGD 
RictorRatlymphangioleiomyomatosis  ISORICTOR (Homo sapiens)protein:increased expression:lung (human)RGD 
RictorMouselymphangioleiomyomatosis  ISORICTOR (Homo sapiens)protein:increased expression:lung (human)RGD 
SLC16A1Humanlymphangioleiomyomatosis  IEP protein:increased expression:lung (human)RGD 
Slc16a1Ratlymphangioleiomyomatosis  ISOSLC16A1 (Homo sapiens)protein:increased expression:lung (human)RGD 
Slc16a1Mouselymphangioleiomyomatosis  ISOSLC16A1 (Homo sapiens)protein:increased expression:lung (human)RGD 
1 to 18 of 18 rows


Genes (Rattus norvegicus)
Acss2  (acyl-CoA synthetase short-chain family member 2) Cpt1a  (carnitine palmitoyltransferase 1A) Gapdh  (glyceraldehyde-3-phosphate dehydrogenase)
Gls  (glutaminase) Rictor  (RPTOR independent companion of MTOR, complex 2) Slc16a1  (solute carrier family 16 member 1)

Genes (Mus musculus)
Acss2  (acyl-CoA synthetase short-chain family member 2) Cpt1a  (carnitine palmitoyltransferase 1a, liver) Gapdh  (glyceraldehyde-3-phosphate dehydrogenase)
Gls  (glutaminase) Rictor  (RPTOR independent companion of MTOR, complex 2) Slc16a1  (solute carrier family 16 (monocarboxylic acid transporters), member 1)

Genes (Homo sapiens)
ACSS2  (acyl-CoA synthetase short chain family member 2) CPT1A  (carnitine palmitoyltransferase 1A) GAPDH  (glyceraldehyde-3-phosphate dehydrogenase)
GLS  (glutaminase) RICTOR  (RPTOR independent companion of MTOR complex 2) SLC16A1  (solute carrier family 16 member 1)