TY - JOUR
T1 - Molecular Research in Pancreatic Cancer
T2 - Small Molecule Inhibitors, Their Mechanistic Pathways and Beyond
AU - Shetu, Shaila A.
AU - James, Nneoma
AU - Rivera, Gildardo
AU - Bandyopadhyay, Debasish
N1 - Publisher Copyright:
© 2023 by the authors.
PY - 2023/3
Y1 - 2023/3
N2 - Pancreatic enzymes assist metabolic digestion, and hormones like insulin and glucagon play a critical role in maintaining our blood sugar levels. A malignant pancreas is incapable of doing its regular functions, which results in a health catastrophe. To date, there is no effective biomarker to detect early-stage pancreatic cancer, which makes pancreatic cancer the cancer with the highest mortality rate of all cancer types. Primarily, mutations of the KRAS, CDKN2A, TP53, and SMAD4 genes are responsible for pancreatic cancer, of which mutations of the KRAS gene are present in more than 80% of pancreatic cancer cases. Accordingly, there is a desperate need to develop effective inhibitors of the proteins that are responsible for the proliferation, propagation, regulation, invasion, angiogenesis, and metastasis of pancreatic cancer. This article discusses the effectiveness and mode of action at the molecular level of a wide range of small molecule inhibitors that include pharmaceutically privileged molecules, compounds under clinical trials, and commercial drugs. Both natural and synthetic small molecule inhibitors have been counted. Anti-pancreatic cancer activity and related benefits of using single and combined therapy have been discussed separately. This article sheds light on the scenario, constraints, and future aspects of various small molecule inhibitors for treating pancreatic cancer—the most dreadful cancer so far.
AB - Pancreatic enzymes assist metabolic digestion, and hormones like insulin and glucagon play a critical role in maintaining our blood sugar levels. A malignant pancreas is incapable of doing its regular functions, which results in a health catastrophe. To date, there is no effective biomarker to detect early-stage pancreatic cancer, which makes pancreatic cancer the cancer with the highest mortality rate of all cancer types. Primarily, mutations of the KRAS, CDKN2A, TP53, and SMAD4 genes are responsible for pancreatic cancer, of which mutations of the KRAS gene are present in more than 80% of pancreatic cancer cases. Accordingly, there is a desperate need to develop effective inhibitors of the proteins that are responsible for the proliferation, propagation, regulation, invasion, angiogenesis, and metastasis of pancreatic cancer. This article discusses the effectiveness and mode of action at the molecular level of a wide range of small molecule inhibitors that include pharmaceutically privileged molecules, compounds under clinical trials, and commercial drugs. Both natural and synthetic small molecule inhibitors have been counted. Anti-pancreatic cancer activity and related benefits of using single and combined therapy have been discussed separately. This article sheds light on the scenario, constraints, and future aspects of various small molecule inhibitors for treating pancreatic cancer—the most dreadful cancer so far.
KW - CDKN2A
KW - Kirsten rat sarcoma oncogene homolog (KRAS)
KW - SMAD4
KW - TP53
KW - natural inhibitors
KW - pancreatic cancer
KW - pancreatic cancer drugs
KW - pancreatic ductal adenocarcinoma
KW - small molecule inhibitors
KW - thymidylate synthase
UR - http://www.scopus.com/inward/record.url?scp=85151154543&partnerID=8YFLogxK
U2 - 10.3390/cimb45030124
DO - 10.3390/cimb45030124
M3 - Artículo de revisión
C2 - 36975494
AN - SCOPUS:85151154543
SN - 1467-3037
VL - 45
SP - 1914
EP - 1949
JO - Current Issues in Molecular Biology
JF - Current Issues in Molecular Biology
IS - 3
ER -