Speaker Biography

Dr. Ekarat Hitakomate

Thammasat University, Pathumthani, Thailand

Title: Inhibition of ribosomal S6 kinase 1 attenuates cell proliferation, migration and invasion of tongue squamous cell carcinoma cells.

Dr. Ekarat Hitakomate
Biography:

Dr. Ekarat Hitakomate received his PhD in cell and molecular biology from the university of Dundee in 2010. His
PhD thesis was focusing on the molecular mechanisms of RCC1 interaction with chromatin and characterization
of its binding partners. His current research interests are biology of oral cancer and the regulation of cancer
metastasis.

Abstract:

Statement of the problem: Tongue squamous cell carcinoma (TSCC) is one of the major health concerns worldwide with high morbidity and mortality rates. Currently, effective therapeutic interventions for TSCC are limited. Therefore, identification of such molecular targets is of clinical relevance. Recent data have shown that the ribosomal protein S6 kinase, 90 kDa, polypeptide 1 (RSK1) a member of Ser/Thr protein kinases plays an important role in regulating cell invasion and metastasis in human cancers. How RSK1 play a role in TSCC remains currently unclear. The purpose of this study was to examine a function of RSK1 in TSCC proliferation, migration, and invasion of the TSCC cell line HSC-3 and its lymph node metastatic counterpart HSC-3-M3 cell line using siRNA approach. Findings: RSK1 expression was efficiently repressed using specific siRNAs compared to that of non-specific siRNA group. We found that silencing RSK1 significantly inhibited cell proliferation in both HSC-3 and HSC-3-M3 cell lines. Live cell migration of HSC-3 and HSC-3-M3 transfected with RSK1 specific siRNA was compared with that of non-specific siRNA transfected cells using live cell imaging. Inhibition of RSK1 expression in both HSC-3 and HSC-3-M3 also affected live cell migration. Importantly, silencing RSK1 interfered with invasive capacity of both HSC-3 and HSC-3-M3 cells lines. How RSK1 is involved in regulating TSCC invasiveness will be discussed. Conclusion & significance: RSK1 may play a role in promoting cell proliferation, cell migration and invasion in TSCC cell lines.

Dr. Ekarat Hitakomate

Thammasat University, Pathumthani, Thailand

Title: Inhibition of ribosomal S6 kinase 1 attenuates cell proliferation, migration and invasion of tongue squamous cell carcinoma cells.

Dr. Ekarat Hitakomate
Biography:

Dr. Ekarat Hitakomate received his PhD in cell and molecular biology from the university of Dundee in 2010. His
PhD thesis was focusing on the molecular mechanisms of RCC1 interaction with chromatin and characterization
of its binding partners. His current research interests are biology of oral cancer and the regulation of cancer
metastasis.

Abstract:

Statement of the problem: Tongue squamous cell
carcinoma (TSCC) is one of the major health concerns
worldwide with high morbidity and mortality rates.
Currently, effective therapeutic interventions for TSCC are
limited. Therefore, identification of such molecular targets
is of clinical relevance. Recent data have shown that the
ribosomal protein S6 kinase, 90 kDa, polypeptide 1
(RSK1) a member of Ser/Thr protein kinases plays an
important role in regulating cell invasion and metastasis in
human cancers. How RSK1 play a role in TSCC remains
currently unclear. The purpose of this study was to
examine a function of RSK1 in TSCC proliferation,
migration, and invasion of the TSCC cell line HSC-3 and
its lymph node metastatic counterpart HSC-3-M3 cell line
using siRNA approach. Findings: RSK1 expression was
efficiently repressed using specific siRNAs compared to
that of non-specific siRNA group. We found that silencing
RSK1 significantly inhibited cell proliferation in both HSC-3
and HSC-3-M3 cell lines. Live cell migration of HSC-3 and
HSC-3-M3 transfected with RSK1 specific siRNA was
compared with that of non-specific siRNA transfected cells
using live cell imaging. Inhibition of RSK1 expression in both
HSC-3 and HSC-3-M3 also affected live cell migration.
Importantly, silencing RSK1 interfered with invasive capacity
of both HSC-3 and HSC-3-M3 cells lines. How RSK1 is
involved in regulating TSCC invasiveness will be discussed.
Conclusion & significance: RSK1 may play a role in
promoting cell proliferation, cell migration and invasion in
TSCC cell lines.

Ekarat Hitakomate

Thammasat University, Thailand

Title: Inhibition of ribosomal S6 kinase 1 attenuates cell proliferation, migration and invasion of tongue squamous cell carcinoma cells

Ekarat Hitakomate
Biography:

Abstract:

Statement of the Problem: Tongue Squamous Cell Carcinoma (TSCC) is one of the major health concerns worldwide with high
morbidity and mortality rates. Currently, effective therapeutic interventions for TSCC are limited. Therefore, identification of such
molecular targets is of clinical relevance. Recent data have shown that the ribosomal protein S6 kinase, 90 kDa, polypeptide 1 (RSK1),
a member of Ser/Thr protein kinases plays an important role in regulating cell invasion and metastasis in human cancers. How RSK1
play a role in TSCC remains currently unclear.
Aim: The purpose of this study was to examine a function of RSK1 in TSCC proliferation, migration and invasion of the TSCC cell
line HSC-3 and its lymph node metastatic counterpart HSC-3-M3 cell line using siRNA approach.
Findings: RSK1 expression was efficiently repressed using specific siRNAs compared to that of non-specific siRNA group. We found
that silencing RSK1 significantly inhibited cell proliferation in both HSC-3 and HSC-3-M3 cell lines. Live cell migration of HSC-3
and HSC-3-M3 transfected with RSK1 specific siRNA was compared with that of non-specific siRNA transfected cells using live cell
imaging. Inhibition of RSK1 expression in both HSC-3 and HSC-3-M3 also affected live cell migration. Importantly, silencing RSK1
interfered with invasive capacity of both HSC-3 and HSC-3-M3 cells lines. How RSK1 is involved in regulating TSCC invasiveness
will be discussed.
Conclusion & Significance: RSK1 may play a role in promoting cell proliferation, cell migration and invasion in TSCC cell lines.