Variability of the Seychelles-Chagos Thermocline Ridge Dynamics in Connection With ENSO and Indian Ocean Dipole
IEEE GEOSCIENCE AND REMOTE SENSING LETTERS
Authors: Burns, Jessica M.; Subrahmanyam, Bulusu
Abstract
Remote processes, such as El Nino-Southern Oscillation (ENSO) and Indian Ocean Dipole (IOD), are primary drivers of the Seychelles-Chagos thermocline ridge (SCTR) interannual variability with respect to ocean temperature and salinity. Although salinity variability in this region is understudied, previous studies have separated out effects of El Nino and IOD on sea surface temperature (SST) anomalies and concluded SST changes due to IOD are primarily associated with the southward advection of warmer equatorial water. Likewise, SST changes due to El Nino are associated with the suppression of clouds over the Indian Ocean. Although ENSO is known to have a stronger impact on SST south of the SCTR (10 degrees S-15 degrees S), this letter finds that the ENSO has a stronger impact on sea surface salinity (SSS) in the SCTR. This letter further explores how the surface and subsurface salinity and temperature in SCTR varies throughout the year in response to ENSO and IOD separate and coevents using long-term Simple Ocean Data Assimilation (SODA) reanalysis records. Our SSS results from the SODA reanalysis are compared and found to be consistent with soil moisture active passive derived SSS observations for both a positive and negative IOD year.
SCTR regulates cell cycle-related genes toward anti-proliferation in normal breast cells while having pro-proliferation activity in breast cancer cells
INTERNATIONAL JOURNAL OF ONCOLOGY
Authors: Kang, Seongeun; Kim, Byungtak; Kang, Han-Sung; Jeong, Gookjoo; Bae, Hansol; Lee, Hyunkyung; Lee, Seungyeon; Kim, Sun Jung
Abstract
Secretin receptor (SCTR), the G-protein coupled receptor (GPCR) for secretin, has been observed to be upregulated in a few tumor types while downregulated in others, promoting or suppressing the proliferation of tumor cells, respectively. However, little is known about the molecular regulatory mechanism of dysregulation in cancer. In the present study, an analysis of the biological pathways affected by methylation in breast cancer using the methylome databases revealed that GPCRs played a major part in the affected pathway. SCTR, one of the dysregulated GPCRs, showed hypermethylation (P<0.01) and downregulation (P<0.05) in breast cancer tissues. Pathway analysis after the downregulation of SCTR by siRNA in MCF-10A cells identified the G2/M stage checkpoint as the top-scored pathway. Cell cycle-related genes were all upregulated or downregulated suppressing cell proliferation. However, the overexpression of SCTR in MCF-7 cells led to a 35% increase of the cell proliferation index and 2.1-fold increase of cellular migration. Our findings indicate that SCTR suppresses the proliferation of normal breast cells, while the gene stimulates the proliferation and migration of cancer cells being downregulated by promoter methylation.