Zhang et al.[17]
|
This study aims to determine the role of ZFAS1 in the regulation of
miR-1271-5p/HK2.
In vitro model:
U251, T98G, A172, LN229 and HS683 glioma cell lines
In vivo model:
Xenograft nude mice injected with U251 cells transfected with
lentivirus vectors containing shZFAS1.
Human Glioma tissues (n=59) from Tongling People’s Hospital, China:
Grade I (n=11), Grade II (n=22), Grade III (n=17) and Grade IV (n=9)
|
Human glioma samples Grades III and IV have higher expression of ZFAS1
than glioma grade I and II.
U251 and T98G cell lines have the highest ZFAS1 expression compared to
A172, LN229 and HS683.
Si-ZFAS1 of U251 and T98G cell lines decreased cell proliferation,
while increasing apoptosis and inhibiting cell invasion. Similarly,
silencing of ZFAS1 reduced tumor growth in xenograft nude mice.
miR-1271-5p expression which was lower in glioma tissues and glioma
cell lines compared to normal brain tissues and NHA, were increased in
si-ZFAS1 transfected cells than in si-NC transfected cells.
ZFAS1 increased the expression of Hexokinase 2 (HK2) in glioma cells
by targeting miR-1271-5p. This is evident where ZFAS1 inhibition
suppressed HK2 expression, and the suppressive effect could be
eliminated by combining it with a miR-1271-5p inhibitor.
ZFAS1 promoted the development of glioma through regulating
miR-1271-5p/HK2 axis by acting as the miR-1271-5p sponge to increase
HK2 expression.
|
Li et al.[57]
|
This study aims to determine the role of ZFAS1 in regulating miR1505p /
PLP2.
In vitro model:
U87, U251, LN229, and T98G cell lines
In vivo model:
Xenograft model-U87 cells expressing sh‐ZFAS1 were injected into
the mice.
Human glioma tissues (n=27) from Nanjing First Hospital, China:
Grade II (n=7), Grade III (n= 10), Grade IV (n=10)
|
ZFAS1 expression is highest in grade IV gliomas.
U87 and U251 cell lines have higher ZFAS1 expression than T98G
and LN229 cell lines.
Knockdown of ZFAS1 increased the susceptibility of U87 and U251
to temozolomide.
miR‐150‐5p expression was lower in glioma tissues than in normal brain
tissues and was shown to be negatively correlated to ZFAS1
expression in glioma tissue.
ZFAS1 promoted proliferation, migration and invasion and
increased resistance to temozolomide in glioma cells by sponging
miR‐150‐5p to regulate Proteolipid protein 2 (PLP2).
ZFAS1 knockdown reduced PLP2 expression, and the inhibitory
effect was partially reversed by miR-150-5p inhibitors.
sh-ZFAS1 significantly inhibited tumour growth in xenograft nude mice
as evident in the reduction of average volume and weight of the
tumours.
|
Yang et al.[36]
|
This study aims to determine the regulation of miR-432-5p by ZFAS1.
In vitro model:
U87, U251, A172 and LN299 glioma cell lines
Human glioma tissue (n=25) from Shanxian Central Hospital, China:
Lower grade glioma; I and II (n=10), High-grade glioma; III and IV
(n=15)
|
U251 and LN229 cells have the highest ZFAS1 expression compared
to U87 and A172.
High ZFAS1 expression was correlated with advanced tumor stage and
shorter overall survival in glioma.
miR‐432‐5p expression was down‐regulated in grade III‐IV gliomas
compared to grade I‐II gliomas. Similarly, miR‐432‐5p expression was
decreased in glioma cell lines.
miR‐432‐5p was suggested to be a target of ZFAS1, where
silencing of ZFAS1 increases the miR‐432‐5p expression, reduced cell
viability, improves cisplatin cytotoxicity while increasing the
apoptosis of U251 and LN229 cells.
This is further confirmed by the downregulation of miR4325p, which
lowered the effects of ZFAS1 knockdown on cisplatin cytotoxicity and
cell viability in glioma cells.
|
Lv et al.[19]
|
This study aims to elucidate the molecular mechanisms of ZFAS1 in
regulating the epithelial– mesenchymal transition (EMT) in glioma
cancer.
In vitro model:
HS683, T98G, U87, and U251 human glioma cell lines
Human glioma tissues (n=69) from First
Affiliated Hospital of Nanchang University, China:
Astrocytomas, n=45; oligodendrogliomas, n=7; ependymomas, n=3; choroid
plexus tumours, n=2, and others, n=8
|
Patients with high ZFAS1 expression exhibited a lower overall survival
time than patients with low ZFAS1 expression, suggesting that ZFAS1
overexpression may serve as an independent prognostic marker for
glioma patients.
ZFAS1 expression level was higher in high grade glioblastoma
cell lines (T98G, U87, and U251) compared with the grade glioma cell
line (HS683)
Si-ZFAS1 suppressed cell proliferation, decreased colony formation,
induced apoptosis, impeded cell migration, and cell invasion in U87
and U251 cells. ZFAS-1 silencing increased the G0/G1 phase of the cell
cycle while decreasing the S phase.
ZFAS1 was proposed to enhance glioma migration and invasion by
promoting EMT progression. This is demonstrated by the negative
correlation between the level of E-cadherin and ZFAS1 expression, as
opposed to other EMT markers, N-cadherin, Integrin β1, ZEB1, and
Twist, which are associated with ZFAS1 expression.
|
Gao et al.[18]
|
This study aims to determine the regulation of epithelial–mesenchymal
transition (EMT) and Notch signaling pathway by ZFAS1.
In vitro model:
U87 and U251 glioma cell lines
Human glioma tissues (n=46) from Affiliated Hospital of Hebei University
of Engineering, China.
|
ZFAS1 expression was upregulated in high grade (III–IV) glioma
compared to low grade (I–II).
ZFAS1 inhibition suppressed the cells proliferation, migration
and invasion, and induced apoptosis in U87 and U251 cells.
ZFAS1 was found to promote glioma development via the EMT and Notch
signalling pathways, where the expression of EMT-related proteins,
E-cadherin, was increased and the expression of proteins N-cadherin
and Snail was decreased in si-ZFAS1 transfected glioma cells, while
Notch signal-related proteins Hes-1 and NICD were decreased.
|