Progastrin peptides increase the risk of developing colonic tumors: Impact on colonic stem cells

Pomila Singh; Shubhashish Sarkar; Carla Kantara; Carrie Maxwell

doi:10.1007/s11888-012-0144-3

Progastrin peptides increase the risk of developing colonic tumors: Impact on colonic stem cells

Pomila Singh, Shubhashish Sarkar, Carla Kantara, Carrie Maxwell

Neuroscience & Cell

Research output: Contribution to journal › Article › peer-review

14 Scopus citations

Abstract

Preneoplastic lesions (aberrant crypt foci, hyperplastic/ dysplastic polyps) are believed to be precursors of sporadic colorectal tumors (adenomas, adenocarcinomas). Aberrant crypt foci and hyperplastic/dysplastic polyps likely originate from abnormal growth of colonic crypts in response to aberrant queues in the microenvironment of colonic crypts. Thus, identifying factors which regulate homeostatic versus aberrant proliferation/apoptosis of colonocytes, especially stem/progenitor cells, may lead to effective preventative/treatment strategies. On the basis of this philosophy, the role of growth factors/peptide hormones potentially available in the circulation/microenvironment of colonic crypts is being examined extensively. Since the time gastrins were discovered as trophic (growth) factors for gastrointestinal cells, the effect of gastrins on the growth of normal/cancer cells has been investigated, leading to many discoveries. Seminal discoveries in the area of gastrins and colon cancer as it relates to molecular pathways associated with formation of colonic tumors are reviewed and the possible impact on diagnostic/preventative/treatment strategies is discussed.

Original language	English (US)
Pages (from-to)	277-289
Number of pages	13
Journal	Current Colorectal Cancer Reports
Volume	8
Issue number	4
DOIs	https://doi.org/10.1007/s11888-012-0144-3
State	Published - Dec 2012

Keywords

Aberrant crypt foci
Adenocarcinomas
Adenomas
Akt
Cancer-stem cells
Cell-surface-associated annexin A2
Chromosomal instability
Cluster of differentiation 133
Cluster of differentiation 44
Colon carcinogenesis
Colonic crypts
Colorectal cancer
CpG island methylator phenotype
Curcumin
Cytochrome c oxidase subunit Vb
Doublecortin-Ca calmodulin kinase like protein
Extracellular-signalregulated kinases
Hyperplastic polyps
Janus kinase
Leucine-rich-repeat-containing G-protein-coupled-receptor 5
Microsatellite-instability
Nuclear factor B
P38 mitogen-activated protein kinase
Phosphoinositide 3-kinase
Progastrin/glycineextended gastrin
Rous Sarcoma viral gene encoded kinase
Signal transducer and activator of transcription 3
β;-Catenin

ASJC Scopus subject areas

Hepatology
Oncology
Gastroenterology

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10.1007/s11888-012-0144-3

Cite this

@article{49ada4527e4f4a5ab901f07d42cb60a9,

title = "Progastrin peptides increase the risk of developing colonic tumors: Impact on colonic stem cells",

abstract = "Preneoplastic lesions (aberrant crypt foci, hyperplastic/ dysplastic polyps) are believed to be precursors of sporadic colorectal tumors (adenomas, adenocarcinomas). Aberrant crypt foci and hyperplastic/dysplastic polyps likely originate from abnormal growth of colonic crypts in response to aberrant queues in the microenvironment of colonic crypts. Thus, identifying factors which regulate homeostatic versus aberrant proliferation/apoptosis of colonocytes, especially stem/progenitor cells, may lead to effective preventative/treatment strategies. On the basis of this philosophy, the role of growth factors/peptide hormones potentially available in the circulation/microenvironment of colonic crypts is being examined extensively. Since the time gastrins were discovered as trophic (growth) factors for gastrointestinal cells, the effect of gastrins on the growth of normal/cancer cells has been investigated, leading to many discoveries. Seminal discoveries in the area of gastrins and colon cancer as it relates to molecular pathways associated with formation of colonic tumors are reviewed and the possible impact on diagnostic/preventative/treatment strategies is discussed.",

keywords = "Aberrant crypt foci, Adenocarcinomas, Adenomas, Akt, Cancer-stem cells, Cell-surface-associated annexin A2, Chromosomal instability, Cluster of differentiation 133, Cluster of differentiation 44, Colon carcinogenesis, Colonic crypts, Colorectal cancer, CpG island methylator phenotype, Curcumin, Cytochrome c oxidase subunit Vb, Doublecortin-Ca calmodulin kinase like protein, Extracellular-signalregulated kinases, Hyperplastic polyps, Janus kinase, Leucine-rich-repeat-containing G-protein-coupled-receptor 5, Microsatellite-instability, Nuclear factor B, P38 mitogen-activated protein kinase, Phosphoinositide 3-kinase, Progastrin/glycineextended gastrin, Rous Sarcoma viral gene encoded kinase, Signal transducer and activator of transcription 3, β;-Catenin",

author = "Pomila Singh and Shubhashish Sarkar and Carla Kantara and Carrie Maxwell",

note = "Funding Information: Acknowledgments P. Singh is supported by NIH grant RO1-CA97959-(9). The authors thank Cheryl Simmons for her valuable secretarial help in preparing the manuscript and Claiborne Fant for helping with the graphic design of the figure.",

year = "2012",

month = dec,

doi = "10.1007/s11888-012-0144-3",

language = "English (US)",

volume = "8",

pages = "277--289",

journal = "Current Colorectal Cancer Reports",

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T1 - Progastrin peptides increase the risk of developing colonic tumors

T2 - Impact on colonic stem cells

AU - Singh, Pomila

AU - Sarkar, Shubhashish

AU - Kantara, Carla

AU - Maxwell, Carrie

N1 - Funding Information: Acknowledgments P. Singh is supported by NIH grant RO1-CA97959-(9). The authors thank Cheryl Simmons for her valuable secretarial help in preparing the manuscript and Claiborne Fant for helping with the graphic design of the figure.

PY - 2012/12

Y1 - 2012/12

N2 - Preneoplastic lesions (aberrant crypt foci, hyperplastic/ dysplastic polyps) are believed to be precursors of sporadic colorectal tumors (adenomas, adenocarcinomas). Aberrant crypt foci and hyperplastic/dysplastic polyps likely originate from abnormal growth of colonic crypts in response to aberrant queues in the microenvironment of colonic crypts. Thus, identifying factors which regulate homeostatic versus aberrant proliferation/apoptosis of colonocytes, especially stem/progenitor cells, may lead to effective preventative/treatment strategies. On the basis of this philosophy, the role of growth factors/peptide hormones potentially available in the circulation/microenvironment of colonic crypts is being examined extensively. Since the time gastrins were discovered as trophic (growth) factors for gastrointestinal cells, the effect of gastrins on the growth of normal/cancer cells has been investigated, leading to many discoveries. Seminal discoveries in the area of gastrins and colon cancer as it relates to molecular pathways associated with formation of colonic tumors are reviewed and the possible impact on diagnostic/preventative/treatment strategies is discussed.

AB - Preneoplastic lesions (aberrant crypt foci, hyperplastic/ dysplastic polyps) are believed to be precursors of sporadic colorectal tumors (adenomas, adenocarcinomas). Aberrant crypt foci and hyperplastic/dysplastic polyps likely originate from abnormal growth of colonic crypts in response to aberrant queues in the microenvironment of colonic crypts. Thus, identifying factors which regulate homeostatic versus aberrant proliferation/apoptosis of colonocytes, especially stem/progenitor cells, may lead to effective preventative/treatment strategies. On the basis of this philosophy, the role of growth factors/peptide hormones potentially available in the circulation/microenvironment of colonic crypts is being examined extensively. Since the time gastrins were discovered as trophic (growth) factors for gastrointestinal cells, the effect of gastrins on the growth of normal/cancer cells has been investigated, leading to many discoveries. Seminal discoveries in the area of gastrins and colon cancer as it relates to molecular pathways associated with formation of colonic tumors are reviewed and the possible impact on diagnostic/preventative/treatment strategies is discussed.

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KW - Adenocarcinomas

KW - Adenomas

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KW - Cancer-stem cells

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KW - Chromosomal instability

KW - Cluster of differentiation 133

KW - Cluster of differentiation 44

KW - Colon carcinogenesis

KW - Colonic crypts

KW - Colorectal cancer

KW - CpG island methylator phenotype

KW - Curcumin

KW - Cytochrome c oxidase subunit Vb

KW - Doublecortin-Ca calmodulin kinase like protein

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KW - Hyperplastic polyps

KW - Janus kinase

KW - Leucine-rich-repeat-containing G-protein-coupled-receptor 5

KW - Microsatellite-instability

KW - Nuclear factor B

KW - P38 mitogen-activated protein kinase

KW - Phosphoinositide 3-kinase

KW - Progastrin/glycineextended gastrin

KW - Rous Sarcoma viral gene encoded kinase

KW - Signal transducer and activator of transcription 3

KW - β;-Catenin

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DO - 10.1007/s11888-012-0144-3

M3 - Article

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SN - 1556-3790

VL - 8

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JO - Current Colorectal Cancer Reports

JF - Current Colorectal Cancer Reports

IS - 4

ER -

Progastrin peptides increase the risk of developing colonic tumors: Impact on colonic stem cells

Abstract

Keywords

ASJC Scopus subject areas

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