Use of RT-PCR to detect co-expression of neuropeptides and their receptors in lung cancer

Ocejo-Garcia, Marta; Ahmed, Samreen; Coulson, Judy M.; Woll, Penella J.

doi:10.1016/s0169-5002(00)00248-8

Cited by 34 publications

(21 citation statements)

References 25 publications

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“…This corresponds to the findings of Ahmed et al (2000) and Ocejo-Garcia et al (2001), who found that ETRs are co-expressed with ET-1 in another human lung adenocarcinoma cell A549. These results indicate that human lung cancer cells both produce ET-1 and express ET A R and ET B R.…”

Section: Discussionsupporting

confidence: 91%

“…In contrast to the results of our study, Ahmed et al (2000) showed that ET A R was downregulated and no Ca 2+ mobilization could be observed in response to ETR stimulation with ET-1 in lung cancer cell lines. The opposite conclusions may result from use of different lung cells expressing different levels of ET-1 and ETRs (Ahmed et al, 2000;Ocejo-Garcia et al, 2001). They also investigated Ca 2+ mobilization in 3/7 small-cell lung cancer cells and 3/4 non-small-cell lung cancer cells not including SPC-A1 cells.…”

Section: Discussionmentioning

confidence: 99%

“…ETRs and endothelin converting enzyme-1 (ECE-1) were also found in several lung cancer cell lines (Cohen et al, 1997a;Ahmed et al, 2000;Ocejo-Garcia et al, 2001). However, at present, no information is available about the biological role of ET-1 in lung cancer cells and its possible cellular mechanism.…”

Section: Introductionmentioning

confidence: 99%

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Endothelin-1 enhances proliferation of lung cancer cells by increasing intracellular free Ca2+

Zhang¹,

Zhou²,

Ye³

2008

Life Sciences

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Endothelin-1 enhances proliferation of lung cancer cells by increasing intracellular free Ca2+

Zhang¹,

Zhou²,

Ye³

2008

Life Sciences

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“…In SCLC, REST is depleted and alternative splicing produces a sNRSF/REST4 isoform lacking one repression domain (1, 16 -19); furthermore, REST corepressors are lost in neuroendocrine NSCLC (20). REST contributes to transcriptional regulation of arginine vasopressin (21), a commonly detected neuropeptide mRNA in SCLC (22) which, together with ANP, could contribute to hyponatremia in some SCLC patients (23). We recently undertook expression profiling in nonneuroendocrine lung cancer cells experimentally depleted of REST to better annotate the REST regulome in lung cancer.…”

mentioning

confidence: 99%

SCG3 Transcript in Peripheral Blood Is a Prognostic Biomarker for REST-Deficient Small Cell Lung Cancer

Moss

Jacobson²,

Walker³

et al. 2008

Clinical Cancer Research

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Purpose: Specific markers of circulating tumor cells may be informative in managing lung cancer.Because the RE-1silencing transcription factor (REST/NRSF) is a transcriptional repressor that is inactivated in neuroendocrine lung cancer, we identified REST-regulated transcripts (CHGA, CHGB, SCG3,VGF, and PCSK1) for evaluation as biomarkers in peripheral blood. Experimental Design: Transcripts were screened across lung cancer and normal cell lines. Candidates were assessed by reverse transcription-PCR and hybridization of RNA extracted from the peripheral blood of 111 lung cancer patients obtained at clinical presentation and from 27 cancer-free individuals. Results: Expression profiling revealed multiple chromogranin transcripts were readily induced on RESTdepletion, most notably SCG3 was induced >500-fold.The SCG3 transcript was also overexpressed by 12,000-fold in neuroendocrine compared with nonneuroendocrine lung cancer cells. In peripheral blood of lung cancer patients and cancer-free individuals, we found that SCG3 was more tumor-specific and more sensitive than other chromogranin transcripts as a biomarker of circulating tumor cells. Overall, 36% of small cell lung cancer (SCLC) and 16% of non-SCLC patients scored positively for normalized SCG3 transcript. This correlated with worse survival among SCLC patients with limited disease (n = 33; P = 0.022) but not extensive disease (n = 29; P = 0.459). Interestingly, the subcohort of 6 SCLC patients with resistance to platinum/ etoposide chemotherapy all scored positively for peripheral blood SCG3 transcript (P = 0.022). Conclusions: SCG3 mRNA, a component of the REST-dependent neurosecretory transcriptional profile, provides a sensitive prognostic biomarker for noninvasive monitoring of neuroendocrine lung cancer.

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“…CCK and gastrin as well as the CCK1R and CCK2R are present in certain cancer cells (Clerc et al, 1997; Coulson et al, 2003; Ocejo-Garcia et al, 2001; Sethi et al, 1993). In SCLC cell lines NCI-H209 and NCI-H345, high affinity CCK binding sites were identified (Yoder and Moody, 1987).…”

Section: Discussionmentioning

confidence: 99%

CI-988 Inhibits EGFR Transactivation and Proliferation Caused by Addition of CCK/Gastrin to Lung Cancer Cells

et al. 2015

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Cholecystokinin (CCK) receptors are G-protein coupled receptors (GPCR) which are present on lung cancer cells. CCK-8 stimulates the proliferation of lung cancer cells, whereas the CCK2R receptor antagonist CI-988 inhibits proliferation. GPCR for some gastrointestinal hormones/neurotransmitters mediate lung cancer growth by causing epidermal growth factor (EGF)R transactivation. Here, the role of CCK/gastrin and CI-988 on EGFR transactivation and lung cancer proliferation were investigated. Addition of CCK-8 or gastrin-17 (100 nM) to NCI-H727 human lung cancer cells increased EGFR Tyr1068 phosphorylation after 2 min. The ability of CCK-8 to cause EGFR tyrosine phosphorylation was blocked by CI-988, gefitinib (EGFR tyrosine kinase inhibitor), PP2 (Src inhibitor), GM6001 (matrix metalloprotease inhibitor) and tiron (superoxide scavenger). CCK-8 nonsulfated and gastrin-17 caused EGFR transactivation and bound with high affinity to NCI-H727 cells, suggesting that the CCK2R is present. CI-988 inhibited the ability of CCK-8 to cause ERK phosphorylation and elevate cytosolic Ca2+. CI-988 or gefitinib inhibited the basal growth of NCI-H727 cells or that stimulated by CCK-8. The results indicate that CCK/gastrin may increase lung cancer proliferation in an EGFR-dependent manner.

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Use of RT-PCR to detect co-expression of neuropeptides and their receptors in lung cancer

Cited by 34 publications

References 25 publications

Endothelin-1 enhances proliferation of lung cancer cells by increasing intracellular free Ca2+

Endothelin-1 enhances proliferation of lung cancer cells by increasing intracellular free Ca2+

SCG3 Transcript in Peripheral Blood Is a Prognostic Biomarker for REST-Deficient Small Cell Lung Cancer

CI-988 Inhibits EGFR Transactivation and Proliferation Caused by Addition of CCK/Gastrin to Lung Cancer Cells

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