Effect of anti-programmed cell death protein-1 antibody combined with paclitaxel on cervical cancer via phosphoinositide 3-kinase/protein kinase b pathway in rats
By: Shi, Chong
.
Contributor(s): Zhang, G.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2021Edition: Vol.83(4), July-Aug.Description: 823-829p.Subject(s): PHARMACEUTICSOnline resources: Click here
In:
Indian journal of pharmaceutical sciencesSummary: The therapeutic effect of combined drugs on cervical cancer has been confirmed. Whether anti-
programmed cell death protein 1 antibody combined with paclitaxel mediates the phosphoinositide
3-kinase-protein kinase B pathway to regulate cervical cancer still needs further research. 20 nude mice
received subcutaneous administration of Henrietta Lacks cells to establish cervical cancer model which was
then assigned into blank control group, control group A (programmed cell death protein 1 antibody (5 mg/
kg) administration), control group B (paclitaxel) and observation group (programmed cell death protein
1 antibody combined with paclitaxel) followed by analysis of cell proliferation, apoptosis, expression of
phosphoinositide 3-kinase-protein kinase B signaling related proteins and messenger ribonucleic acids.
Observation group had lowest tumor size, highest cell proliferation inhibition rate and cell apoptosis,
which were all reversed in blank group with largest tumor size, lowest cell proliferation inhibition rate
and cell apoptosis. There was no difference between control group A and control group B (p>0.05). The
expressions of phosphoinositide 3-kinase, protein kinase B, tumor protein p53 and tumor protein p21 were
lowest in observation group and highest in blank group. In addition, control group had no significant
difference with control group B (p>0.05). Anti-programmed cell death protein 1 antibody combined
with paclitaxel may inhibit the activity of phosphoinositide 3-kinase-protein kinase B signaling, thereby
downregulating phosphoinositide 3-kinase, protein kinase B, tumor protein p53 and tumor protein p21,
controlling cervical cancer cell division, promoting cell apoptosis and finally exerting anti-tumor effects.
| Item type | Current location | Call number | Status | Date due | Barcode | Item holds |
|---|---|---|---|---|---|---|
Articles Abstract Database
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School of Pharmacy Archieval Section | Not for loan | 2022-0935 |
The therapeutic effect of combined drugs on cervical cancer has been confirmed. Whether anti-
programmed cell death protein 1 antibody combined with paclitaxel mediates the phosphoinositide
3-kinase-protein kinase B pathway to regulate cervical cancer still needs further research. 20 nude mice
received subcutaneous administration of Henrietta Lacks cells to establish cervical cancer model which was
then assigned into blank control group, control group A (programmed cell death protein 1 antibody (5 mg/
kg) administration), control group B (paclitaxel) and observation group (programmed cell death protein
1 antibody combined with paclitaxel) followed by analysis of cell proliferation, apoptosis, expression of
phosphoinositide 3-kinase-protein kinase B signaling related proteins and messenger ribonucleic acids.
Observation group had lowest tumor size, highest cell proliferation inhibition rate and cell apoptosis,
which were all reversed in blank group with largest tumor size, lowest cell proliferation inhibition rate
and cell apoptosis. There was no difference between control group A and control group B (p>0.05). The
expressions of phosphoinositide 3-kinase, protein kinase B, tumor protein p53 and tumor protein p21 were
lowest in observation group and highest in blank group. In addition, control group had no significant
difference with control group B (p>0.05). Anti-programmed cell death protein 1 antibody combined
with paclitaxel may inhibit the activity of phosphoinositide 3-kinase-protein kinase B signaling, thereby
downregulating phosphoinositide 3-kinase, protein kinase B, tumor protein p53 and tumor protein p21,
controlling cervical cancer cell division, promoting cell apoptosis and finally exerting anti-tumor effects.
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