GC |
Enhanced metastasis |
Nicotine and its derived nitrosamine compound (i.e. NNK) through activation of α7nAChR-related signaling pathways significantly enhanced gastric cancer (GC) metastasis. |
[56, 57] |
GC |
Induced proliferation |
Exposure to nicotine and NNK via α7nAChR mechanisms significantly induced cell proliferation in the AGS cell line. |
[58] |
GC |
Enhanced chemosensitivity |
α7nAChR enhanced the sensitivity of cancerous cells to chemotherapeutic reagents including taxanes and ixabepilone. |
[6, 59] |
GC |
Enhanced chemoresistance |
Targeted delivery of siRNA against α7nAChR makes gastric tumor cells became more resistant to 5-FU treatment. |
[73] |
CRC |
Induced proliferation |
Nicotine promotes cell proliferation via α7nAChR in human colorectal cancer (CRC) cell line. |
[7] |
CRC |
Enhanced migration |
Nicotine and tobacco-specific carcinogen (NNK) enhanced CRC cells migration through α7nAChR-mediated mechanisms. |
[42, 43] |
CRC |
Enhanced tumor growth |
ACh itself via α7nAChR serves as an important autocrine/paracrine growth factor in the human colon adenocarcinoma cell line HT-29. |
[44] |
CRC |
Suppressed tumorigenesis |
Nicotine suppresses acute colitis and CRC associated with chronic colitis in mice an effect that attenuated by the antagonist of α7nAChR. |
[49] |
CRC |
Suppressed metastasis |
α7nAChR in tumor-associated macrophages inhibits CRC metastasis in both animal model and LoVo human CRC cell line. |
[52, 53] |
PC |
Induced proliferation |
Nicotine and its nitrosated carcinogenic derivatives, promote cell proliferation of pancreatic cancer (PC) through activation of α7nAChR. |
[8] |
PC |
Induced CSCs renewal |
Nicotine induces self-renewal of pancreatic cancer stem cells (CSCs) through α7nAChR dependent mechanisms. |
[92] |
PC |
Enhanced metastasis |
Nicotine and cigarette-smoke promote the metastasis of PC via α7nAChR downstream signaling cascades. |
[93] |
LC |
Induced proliferation |
Nicotine acts through α7nAChR to stimulate the cholangiocyte proliferation in a xenograft mice model of liver cancer (LC). |
[78] |
LC |
Increased carcinogenesis |
NNK through increased expression of α7nAChR caused hepatic damage and LC progression in an experimental animal model. |
[79] |
LC |
Enhanced tumor growth |
Nicotine-triggered α7nAChR activation promotes both in vitro and in vivo tumor growth of HCC cells. |
[81] |