| + |
ANXA3 | up-regulates activity 
|
NFKBIA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262213 |
|
|
Homo sapiens |
A-549 Cell |
| pmid |
sentence |
| 27995049 |
We also investigated the potential regulation of cancer-associated signaling pathways by Anxa3 through screening for the altered expression of some common signaling molecules after Anxa3 downregulation. Decreased phosphorylation of MEK1/2, ERK1/2, Akt, and IκBα was detected after downregulating Anxa3 expression in A549 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ANXA3 | up-regulates activity
|
AKT |
0.286 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262212 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27995049 |
We also investigated the potential regulation of cancer-associated signaling pathways by Anxa3 through screening for the altered expression of some common signaling molecules after Anxa3 downregulation. Decreased phosphorylation of MEK1/2, ERK1/2, Akt, and IκBα was detected after downregulating Anxa3 expression in A549 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ANXA3 | up-regulates activity
|
JNK |
0.282 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262214 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26095609 |
ANXA3 Induces a Feed-Forward Loop that Is Mediated by the MKK4/JNK Signaling Cascade. To substantiate the importance of the JNK/AP-1 pathway in ANXA3-driven HCC, we performed rescue experiments using the JNK-specific inhibitor (JNKi) SP600125. JNKi suppressed the oncogenic properties conferred by ANXA3 overexpression, as evidenced by the diminished abilities of HCC cells to form colonies, migrate, invade, induce angiogenesis, form hepatospheres, and resist apoptosis and chemotherapy (Figures 6F–6J). Interestingly, treatment of parental HCC cells or HCC cells overexpressing ANXA3 with JNKi resulted in not only a reduction in JNK activity and modulation of downstream target genes (c-MYC and p21) but also a marked decrease in ANXA3 expression, suggesting that ANXA3 induces a feed-forward loop that is mediated by MKK4/JNK signaling (Figures 6K–6L). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ANXA3 | down-regulates 
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262208 |
|
|
Homo sapiens |
HCT-116 Cell, SW-480 Cell |
| pmid |
sentence |
| 30998268 |
ANXA3 downregulation evidently increased the apoptosis of HCT116 (Figure 2C) and SW480 (Figure 2D) cells, and Ox‐induced cell apoptosis was further aggravated by ANXA3 suppression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JNK | up-regulates quantity by expression
transcriptional regulation
|
ANXA3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262216 |
|
|
Homo sapiens |
Hepatoma Cell |
| pmid |
sentence |
| 26095609 |
ANXA3 Induces a Feed-Forward Loop that Is Mediated by the MKK4/JNK Signaling Cascade. To substantiate the importance of the JNK/AP-1 pathway in ANXA3-driven HCC, we performed rescue experiments using the JNK-specific inhibitor (JNKi) SP600125. JNKi suppressed the oncogenic properties conferred by ANXA3 overexpression, as evidenced by the diminished abilities of HCC cells to form colonies, migrate, invade, induce angiogenesis, form hepatospheres, and resist apoptosis and chemotherapy (Figures 6F–6J). Interestingly, treatment of parental HCC cells or HCC cells overexpressing ANXA3 with JNKi resulted in not only a reduction in JNK activity and modulation of downstream target genes (c-MYC and p21) but also a marked decrease in ANXA3 expression, suggesting that ANXA3 induces a feed-forward loop that is mediated by MKK4/JNK signaling (Figures 6K–6L). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ANXA3 | up-regulates activity
|
ERK1/2 |
0.281 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262211 |
|
|
Homo sapiens |
A-549 Cell |
| pmid |
sentence |
| 27995049 |
We also investigated the potential regulation of cancer-associated signaling pathways by Anxa3 through screening for the altered expression of some common signaling molecules after Anxa3 downregulation. Decreased phosphorylation of MEK1/2, ERK1/2, Akt, and IκBα was detected after downregulating Anxa3 expression in A549 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CAV1 | up-regulates quantity
relocalization
|
ANXA3 |
0.295 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262215 |
|
|
Homo sapiens |
Hepatoma Cell |
| pmid |
sentence |
| 26095609 |
There has been no study regarding the route of entry of exogenous ANXA3 in any cell type thus far. We found exogenous ANXA3 to be internalized into HCC cells through caveolin-1-mediated, but not HSPG-mediated, endocytosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ANXA3 | up-regulates activity
|
MEK1/2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262210 |
|
|
Homo sapiens |
A-549 Cell |
| pmid |
sentence |
| 27995049 |
We also investigated the potential regulation of cancer-associated signaling pathways by Anxa3 through screening for the altered expression of some common signaling molecules after Anxa3 downregulation. Decreased phosphorylation of MEK1/2, ERK1/2, Akt, and IκBα was detected after downregulating Anxa3 expression in A549 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ANXA3 | down-regulates quantity by repression
transcriptional regulation
|
CASP3 |
0.266 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262209 |
|
|
Homo sapiens |
HCT-116 Cell, SW-480 Cell |
| pmid |
sentence |
| 30998268 |
ANXA3 depletion promoted cell apoptosis and upregulated c‐caspase 3 expression in HCT116/Ox and SW480/Ox cells with or without Ox, which is consistent with findings from a preliminary study by Yan et al |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
ANXA3
- 
- 