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Wnt Signaling-Related Long Noncoding RNAs: Critical Mediators of Drug Resistance in Colon Cancer

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Colon Cancer Diagnosis and Therapy Vol. 3
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Abstract

Colon cancer is the third largest cancer-related death in the world and is increasing in developing countries. Several molecular pathways controlled by multiple molecules and genes are reported to be involved in colon cancer development. Wnt signaling is recognized as a hallmark of colon cancer. It is a critical regulator of the early and late stages of colon cancer metastasis. Emerging studies have suggested that most human genomes have been transcribed as long noncoding RNA (lncRNA). This chapter presents the current status of colon cancer worldwide, therapeutic options for targeting metastasis, and the importance of the Wnt signaling pathway in colon cancer metastasis and describes the downregulated and upregulated lncRNA in colon cancer. This chapter also uncovers the role of Wnt signaling pathway-related lncRNAs in drug resistance and metastasis of colon cancer cells. Finally, this chapter discusses phytochemical therapeutics for targeting Wnt pathway-related lncRNAs in colon cancer. In conclusion, Wnt pathway-related lncRNAs that modulate the diverse mechanisms of drug resistance and metastatic ability of colon cancer are potential targets of phytochemical therapeutics.

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Abbreviations

5-FU:

5-fluorouracil

ABC:

ATP-binding cassette

APC:

Adenomatous polyposis coli

ATP:

Adenosine triphosphate

B3GALT5-AS1:

Beta-1,3-GalTase 5 anti-sense

Bax:

Bcl 2-associated X

Bcl2:

B-cell lymphoma 2

BRAF:

B-Raf

CASC15:

Cancer susceptibility 15

CC:

Colon cancer

CCAT1:

Colon cancer-associated transcript 1

CCAT2:

Colon cancer-associated transcript 2

CD133:

Cluster of differentiation 133

CD44:

Cluster of differentiation 44

CK1:

Casein kinase 1

CPT:

Camptothecin

CRC:

Colorectal cancers

CRNDE:

Colorectal neoplasia differentially expressed

CUR:

Curcumin

CYTOR:

Cytoskeleton regulator RNA

DNA:

Deoxyribonucleic acid

EGCG:

Epigallocatechin-3-gallate

EGFR:

Epithelial growth factor receptor

EMT:

Epithelial-to-mesenchymal transition

GEN:

Genistein, quercetin

GSK-3 β:

Glycogen synthase kinase 3 β

GWAS:

Genome-wide association studies

HOTAIR:

HOX transcript antisense RNA

HULC:

Highly upregulated in liver cancer

K-ras :

Kirsten rat sarcoma virus

LGR5:

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

LIFR-AS1:

Leukemia inhibitory factor receptor-antisense 1

lncRNAs:

Long noncoding RNAs

MALAT1:

Metastasis-associated lung adenocarcinoma transcript 1

MAP:

myh-associated polyposis (MAP)

MAPK:

Mitogen-activated protein kinase

MDRP 1:

Multidrug-resistant protein 1

miRNAs:

microRNAs

MLH1:

mutL homolog 1

MMP9:

Matrix metalloproteinase9

MRP1:

Multidrug resistance protein 1

NATs:

Natural antisense transcripts

NF-κB:

Nuclear factor κ B

OX:

Oxaliplatin

PDT:

Photodynamic therapy

P-gp:

p-glycoprotein

PI3K:

Phosphatidylinositol 3-kinase

PTEN:

Phosphatase and tensin homolog

RNAi:

RNA interference

RSV:

Resveratrol

SLAIN2:

Slain motif-containing protein 2

SLC:

Solute carrier

STARD13-AS:

StAR-related lipid transfer domain 13 antisense

TCF:

T-cell factor

TEM:

Transanal endoscopic microsurgery

TGF-β:

Transformation growth factor-β

TP53:

Tumor protein 53

UCA1:

Urothelial carcinoma-associated 1

VEGF-A:

Vascular endothelial growth factor-A

Wnt:

Wingless-related integration site

YAP1:

Yes-associated protein 1

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Acknowledgments

The authors thank the GITAM management for providing the infrastructural facilities.

Funding Details

The corresponding author, Prof. RamaRao Malla (receiver of the grant), thanks CSIR, New Delhi, India (file no. 37(1683)/17/EMR-II; dated: 05.05.2017), for providing funding to carry out this work.

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The authors declare that there is no conflict of interest.

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Raju, P.V., Malla, R. (2022). Wnt Signaling-Related Long Noncoding RNAs: Critical Mediators of Drug Resistance in Colon Cancer. In: Shukla, D., Vishvakarma, N.K., Nagaraju, G.P. (eds) Colon Cancer Diagnosis and Therapy Vol. 3. Springer, Cham. https://doi.org/10.1007/978-3-030-72702-4_2

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