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TAF1L promotes development of oral squamous cell carcinoma via decreasing autophagy-dependent apoptosis

Identifieur interne : 001019 ( Ncbi/Merge ); précédent : 001018; suivant : 001020

TAF1L promotes development of oral squamous cell carcinoma via decreasing autophagy-dependent apoptosis

Auteurs : Daiwei Wang [République populaire de Chine] ; Hong Qi [République populaire de Chine] ; Haoxing Zhang [République populaire de Chine] ; Wei Zhou [République populaire de Chine] ; Yanpeng Li [République populaire de Chine] ; Ang Li [République populaire de Chine] ; Qiong Liu [République populaire de Chine] ; Yun Wang [République populaire de Chine]

Source :

RBID : PMC:7053316

Abstract

This study focused on investigating the relationships of TAF1L expression and clinical features or pathological stages of oral squamous cell carcinoma (OSCC), and its potential roles of TAF1L on OSCC development. Western blot and immunohistochemical staining were used to detect TAF1L expression in OSCC tissues and cells. Effects of TAF1L on OSCC cells in vitro were examined by cell proliferation assay, wound healing assay, transwell chamber assay, flow cytometry analysis and siRNA technique. Cellular key proteins related to cell autophagy and apoptosis were evaluated by Western blot and immunofluorescent staining. Moreover, functions of TAF1L on OSCC process were observed in nude mouse model. Testing results showed that expression of TAF1L protein was higher in OSCC tissues than that in normal oral epithelial or paracancerous tissues. Additionally, the level of TAF1L protein expression was upregulated in OSCC cell lines, compared to that in normal oral epithelial cells. Furthermore, cell proliferation, migration, autophagy and apoptosis were modulated post siRNA-TAF1L treatment in vitro. Especially, TAF1L knockdown-induced apoptotic activation on OSCC cells could be rescued by autophagic activator (Rapamycin). Moreover, that overexpression of TAF1L protein could promote the growth of OSCC cell xenografts was confirmed in nude mouse model. Taken together, it suggests that TAF1L may facilitate OSCC cells to escape cell apoptosis via autophagic activation for enhancing OSCC development.


Url:
DOI: 10.7150/ijbs.41148
PubMed: 32174793
PubMed Central: 7053316

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<p>This study focused on investigating the relationships of TAF1L expression and clinical features or pathological stages of oral squamous cell carcinoma (OSCC), and its potential roles of TAF1L on OSCC development. Western blot and immunohistochemical staining were used to detect TAF1L expression in OSCC tissues and cells. Effects of TAF1L on OSCC cells
<italic> in vitro</italic>
were examined by cell proliferation assay, wound healing assay, transwell chamber assay, flow cytometry analysis and siRNA technique. Cellular key proteins related to cell autophagy and apoptosis were evaluated by Western blot and immunofluorescent staining. Moreover, functions of TAF1L on OSCC process were observed in nude mouse model. Testing results showed that expression of TAF1L protein was higher in OSCC tissues than that in normal oral epithelial or paracancerous tissues. Additionally, the level of TAF1L protein expression was upregulated in OSCC cell lines, compared to that in normal oral epithelial cells. Furthermore, cell proliferation, migration, autophagy and apoptosis were modulated post siRNA-
<italic>TAF1L</italic>
treatment
<italic>in vitro</italic>
. Especially, TAF1L knockdown-induced apoptotic activation on OSCC cells could be rescued by autophagic activator (Rapamycin). Moreover, that overexpression of TAF1L protein could promote the growth of OSCC cell xenografts was confirmed in nude mouse model. Taken together, it suggests that TAF1L may facilitate OSCC cells to escape cell apoptosis via autophagic activation for enhancing OSCC development.</p>
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</TEI>
<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Int J Biol Sci</journal-id>
<journal-id journal-id-type="iso-abbrev">Int. J. Biol. Sci</journal-id>
<journal-id journal-id-type="publisher-id">ijbs</journal-id>
<journal-title-group>
<journal-title>International Journal of Biological Sciences</journal-title>
</journal-title-group>
<issn pub-type="epub">1449-2288</issn>
<publisher>
<publisher-name>Ivyspring International Publisher</publisher-name>
<publisher-loc>Sydney</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">32174793</article-id>
<article-id pub-id-type="pmc">7053316</article-id>
<article-id pub-id-type="doi">10.7150/ijbs.41148</article-id>
<article-id pub-id-type="publisher-id">ijbsv16p1180</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Research Paper</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>TAF1L promotes development of oral squamous cell carcinoma via decreasing autophagy-dependent apoptosis</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Wang</surname>
<given-names>Daiwei</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Qi</surname>
<given-names>Hong</given-names>
</name>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zhang</surname>
<given-names>Haoxing</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zhou</surname>
<given-names>Wei</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Li</surname>
<given-names>Yanpeng</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Li</surname>
<given-names>Ang</given-names>
</name>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Liu</surname>
<given-names>Qiong</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Wang</surname>
<given-names>Yun</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="corresp" rid="FNA_envelop"></xref>
</contrib>
</contrib-group>
<aff id="A1">
<label>1</label>
Center for Research and Technology of Precision Medicine, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, Guangdong, China.</aff>
<aff id="A2">
<label>2</label>
Key Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering, Shenzhen University, Shenzhen, Guangdong, China.</aff>
<aff id="A3">
<label>3</label>
Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University. Xi'an, Shanxi, China</aff>
<author-notes>
<corresp id="FNA_envelop">✉ Corresponding author: Center for Research and Technology of Precision Medicine, College of Life Sciences and Oceanography, Shenzhen University (Lihu Campus), No. 1066, Xueyuan Ave, Nanshan Distract, Shenzhen, Guangdong (518055), P.R.China. Email address:
<email>yunw@szu.edu.cn</email>
.</corresp>
<fn fn-type="COI-statement">
<p>Competing Interests: The authors have declared that no competing interest exists.</p>
</fn>
</author-notes>
<pub-date pub-type="collection">
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>10</day>
<month>2</month>
<year>2020</year>
</pub-date>
<volume>16</volume>
<issue>7</issue>
<fpage>1180</fpage>
<lpage>1193</lpage>
<history>
<date date-type="received">
<day>14</day>
<month>10</month>
<year>2019</year>
</date>
<date date-type="accepted">
<day>26</day>
<month>12</month>
<year>2019</year>
</date>
</history>
<permissions>
<copyright-statement>© The author(s)</copyright-statement>
<copyright-year>2020</copyright-year>
<license license-type="open-access">
<license-p>This is an open access article distributed under the terms of the Creative Commons Attribution License (
<ext-link ext-link-type="uri" xlink:href="https://creativecommons.org/licenses/by/4.0/">https://creativecommons.org/licenses/by/4.0/</ext-link>
). See
<ext-link ext-link-type="uri" xlink:href="http://ivyspring.com/terms">http://ivyspring.com/terms</ext-link>
for full terms and conditions.</license-p>
</license>
</permissions>
<abstract>
<p>This study focused on investigating the relationships of TAF1L expression and clinical features or pathological stages of oral squamous cell carcinoma (OSCC), and its potential roles of TAF1L on OSCC development. Western blot and immunohistochemical staining were used to detect TAF1L expression in OSCC tissues and cells. Effects of TAF1L on OSCC cells
<italic> in vitro</italic>
were examined by cell proliferation assay, wound healing assay, transwell chamber assay, flow cytometry analysis and siRNA technique. Cellular key proteins related to cell autophagy and apoptosis were evaluated by Western blot and immunofluorescent staining. Moreover, functions of TAF1L on OSCC process were observed in nude mouse model. Testing results showed that expression of TAF1L protein was higher in OSCC tissues than that in normal oral epithelial or paracancerous tissues. Additionally, the level of TAF1L protein expression was upregulated in OSCC cell lines, compared to that in normal oral epithelial cells. Furthermore, cell proliferation, migration, autophagy and apoptosis were modulated post siRNA-
<italic>TAF1L</italic>
treatment
<italic>in vitro</italic>
. Especially, TAF1L knockdown-induced apoptotic activation on OSCC cells could be rescued by autophagic activator (Rapamycin). Moreover, that overexpression of TAF1L protein could promote the growth of OSCC cell xenografts was confirmed in nude mouse model. Taken together, it suggests that TAF1L may facilitate OSCC cells to escape cell apoptosis via autophagic activation for enhancing OSCC development.</p>
</abstract>
<kwd-group>
<kwd>TAF1L</kwd>
<kwd>OSCC</kwd>
<kwd>apoptosis</kwd>
<kwd>autophagy</kwd>
<kwd>siRNA</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group>
<fig id="F1" position="float">
<label>Figure 1</label>
<caption>
<p>The levels of TAF1L protein expression in OSCC tissues and normal oral/paracancerous tissues were observed by IHC. A, TAF1L overexpression in OSCC tissues vs. TAF1L lower expression in normal tissues. Scale bars: 20 μm. B, Quantification of the mean scores of TAF1L positive signals between OSCC tissues and normal oral epithelial tissues. C, Overexpression of TAF1L in OSCC tissues was showed at different TNM-T stages, compared with normal oral epithelial tissues. Brown color showed positive signals. Scale bars: 20 μm in the top row and 100 μm in the bottom row. D, The means of density scores of TAF1L were showed higher at different TNM-T stages of OSCC, compared with normal oral epithelial tissues. OSCC tissues: n = 110, normal oral/paracancerous tissues: n = 30. Positive signals were showed with brown color. ***
<italic>p</italic>
< 0.0001 (one-way ANOVA).</p>
</caption>
<graphic xlink:href="ijbsv16p1180g001"></graphic>
</fig>
<fig id="F2" position="float">
<label>Figure 2</label>
<caption>
<p>The levels of TAF1L protein expression of OSCC cells after
<italic>TAF1L</italic>
gene knockdown with siRNA technique were detected by Western blot and CCK-8 assays. A, TAF1L protein expression of a panel of OSCC cells was showed with special antibody against TAF1L antigen. B, TAF1L protein level related to (A) was measured based on the intensity of Western blot. C, Cells were detected after 48 hr transfection with selected siRNA-
<italic>TAF1L</italic>
or siRNA-control. Verification of
<italic>TAF1L</italic>
gene knockdown post siRNA treatment in Ca9-22 cells or Tca-8113 cells was via Western blot with antibody against TAF1L or GAPDH. D, Downregulation of TAF1L was tested at the protein level related to (C). E, Using the CCK-8 assay and cell proliferation were measured in Tca-8113 cells and Ca9-22 cells after siRNA-
<italic>TAF1L</italic>
(TAF1L-KD) or siRNA-control transfection for time response. Cell viability was determined at scheduled time point. Data were showed Mean ± SD, N = 3,
<italic>
<sup>*</sup>
p</italic>
< 0.01,
<italic>
<sup>**</sup>
p</italic>
< 0.001,
<italic>
<sup>***</sup>
p</italic>
< 0.0001 (Student's
<italic>t</italic>
-test).</p>
</caption>
<graphic xlink:href="ijbsv16p1180g002"></graphic>
</fig>
<fig id="F3" position="float">
<label>Figure 3</label>
<caption>
<p>The migration and invasion of OSCC cells were decreased by siRNA-
<italic>TAF1L</italic>
treatment. A, Cell migration into the open space was monitored. Scale bars: 100 μm. B, Quantification of the length of migration was generated at appoint time after wounding was made from (A). C, Cell numbers for measuring the invasion were counted via transwell invasion assay. Scale bars: 100 μm. D, Those invading cells were counted, and compared with those obtained from (C) for quantified analysis. Scale bars: 100 μm, Student's
<italic>t</italic>
-test: Mean ± SD, N=3, **
<italic>p</italic>
< 0.001, ***
<italic>p</italic>
< 0.0001.</p>
</caption>
<graphic xlink:href="ijbsv16p1180g003"></graphic>
</fig>
<fig id="F4" position="float">
<label>Figure 4</label>
<caption>
<p>Apoptosis of OSCC cells were evaluated by
<italic>TAF1L</italic>
gene silence. A and B: The rates of cell apoptosis were observed in Tca-8113 cells (A) and Ca9-22 cells (B) transfected siRNA-
<italic>TAF1L</italic>
(
<italic>TAF1L</italic>
-KD) under a flow cytometer. C: Effects of
<italic>TAF1L</italic>
gene knockdown on cell apoptosis related Caspase-3 protein in Tca-8113 cells and Ca9-22 cells were detected with Western blot. D: Effects of
<italic>TAF1L</italic>
gene knockdown on apoptosis related Bax and Bcl-2 proteins in Tca-8113 and Ca9-22 cells were evaluated with Western blot. Protein quantification: Mean ± SD, N = 3,
<italic>
<sup>*</sup>
p</italic>
< 0.01,
<italic>
<sup>**</sup>
p</italic>
< 0.001 (Student's
<italic>t</italic>
-test).</p>
</caption>
<graphic xlink:href="ijbsv16p1180g004"></graphic>
</fig>
<fig id="F5" position="float">
<label>Figure 5</label>
<caption>
<p>Effects of
<italic>TAF1L</italic>
gene depletion on cell autophagy were showed in OSCC cells. A, Autophagy-related proteins (LC3B and p62) were detected post
<italic>TAF1L</italic>
gene knockdown by Western blot. B, Proteins quantification was related to (A). C,
<bold> A</bold>
utophagic activity was assayed via confocal microscopy with immunolabeling for autophagy-related LC3B-GFP (green color). Scale bars: 5μm. D, Quantification of the ratio of green dot area (LC3B-GFP) to total cell area in (C). >30 cells per condition from three independent experiments were analyzed. Mean ± SD, N = 3,
<italic>
<sup>*</sup>
p</italic>
< 0.01,
<italic>
<sup>**</sup>
p</italic>
< 0.001,
<italic>
<sup>***</sup>
p</italic>
< 0.0001 (Student's
<italic>t</italic>
-test).</p>
</caption>
<graphic xlink:href="ijbsv16p1180g005"></graphic>
</fig>
<fig id="F6" position="float">
<label>Figure 6</label>
<caption>
<p>
<italic>TAF1L</italic>
gene silence-induced apoptosis in OSCC cells could be rescued by the Rapamycin treatment. The Ca9-22 and Tca8113 cells were divided into two groups based on siRNA-
<italic>TAF1L</italic>
or siRNA-control treatment, and then treated with 0.1 μM Rapamycin (Rapa) or the diluent with same concentration of dimethyl sulphoxide (DMSO) for 16 hr. A, Autophagy- and apoptosis-related markers (e.g., LC3B, p62 and Caspase-3) were tested with Western blot. B, Levels of protein expression in (A) were shown up (Mean ± SD, N = 3,
<italic>
<sup>*</sup>
p</italic>
< 0. 01, one-way ANOVA). C-D, By flow cytometry, the image on the left showed changes of apoptotic cell ratios in Tca-8113 cells (C) and Ca9-22 cells (D), and on the right one showed percentages of apoptotic cell in the same cell line. Mean ± SD, N = 3, *
<italic>p</italic>
< 0.01, **
<italic>p</italic>
< 0.001, ***
<italic>p</italic>
< 0.0001 (Student's
<italic>t</italic>
-test).</p>
</caption>
<graphic xlink:href="ijbsv16p1180g006"></graphic>
</fig>
<fig id="F7" position="float">
<label>Figure 7</label>
<caption>
<p>TAF1L overexpression promoted OSCC tumor growth
<italic> in vivo</italic>
. A, Female nude mice (left) and tumor xenograftes (right) were represented at 35 days post subcutaneous injection. B, The curves of tumor volume in nude mice were showed up (
<italic>
<sup>***</sup>
p</italic>
< 0. 001, Student's
<italic>t</italic>
-test). C, The curves of tumor weight were represented at 35 days post subcutaneous injection,
<italic>
<sup>*</sup>
p</italic>
< 0.05 (Student's
<italic>t-</italic>
test). D, Comparison of TAF1L, apoptosis and autophagy markers expressions in the xenograft model. Scale bars: 100 μm.</p>
</caption>
<graphic xlink:href="ijbsv16p1180g007"></graphic>
</fig>
<table-wrap id="T1" position="float">
<label>Table 1</label>
<caption>
<p>Clinical characteristics of OSCC patients obtained in this study</p>
</caption>
<table frame="hsides" rules="groups">
<thead valign="top">
<tr>
<th rowspan="1" colspan="1">Parameters</th>
<th rowspan="1" colspan="1">Case numbers (n)</th>
<th rowspan="1" colspan="1">%</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td rowspan="1" colspan="1">
<bold>Age (years)</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">≤50</td>
<td rowspan="1" colspan="1">37</td>
<td rowspan="1" colspan="1">61.82</td>
</tr>
<tr>
<td rowspan="1" colspan="1">>50</td>
<td rowspan="1" colspan="1">73</td>
<td rowspan="1" colspan="1">39.18</td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>Gender</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">Female</td>
<td rowspan="1" colspan="1">42</td>
<td rowspan="1" colspan="1">38.18</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Male</td>
<td rowspan="1" colspan="1">68</td>
<td rowspan="1" colspan="1">61.82</td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>Histological differentiation</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">Well</td>
<td rowspan="1" colspan="1">81</td>
<td rowspan="1" colspan="1">73.64</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Moderate</td>
<td rowspan="1" colspan="1">15</td>
<td rowspan="1" colspan="1">13.64</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Poor</td>
<td rowspan="1" colspan="1">21</td>
<td rowspan="1" colspan="1">19.09</td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>Clinical stage</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">I</td>
<td rowspan="1" colspan="1">20</td>
<td rowspan="1" colspan="1">33.33</td>
</tr>
<tr>
<td rowspan="1" colspan="1">II</td>
<td rowspan="1" colspan="1">24</td>
<td rowspan="1" colspan="1">40</td>
</tr>
<tr>
<td rowspan="1" colspan="1">III</td>
<td rowspan="1" colspan="1">5</td>
<td rowspan="1" colspan="1">8.33</td>
</tr>
<tr>
<td rowspan="1" colspan="1">IV</td>
<td rowspan="1" colspan="1">1</td>
<td rowspan="1" colspan="1">1.67</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Unknown</td>
<td rowspan="1" colspan="1">10</td>
<td rowspan="1" colspan="1">16.67</td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>T classification</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">T1</td>
<td rowspan="1" colspan="1">45</td>
<td rowspan="1" colspan="1">40.91</td>
</tr>
<tr>
<td rowspan="1" colspan="1">T2</td>
<td rowspan="1" colspan="1">43</td>
<td rowspan="1" colspan="1">39.09</td>
</tr>
<tr>
<td rowspan="1" colspan="1">T3</td>
<td rowspan="1" colspan="1">9</td>
<td rowspan="1" colspan="1">8.18</td>
</tr>
<tr>
<td rowspan="1" colspan="1">T4</td>
<td rowspan="1" colspan="1">11</td>
<td rowspan="1" colspan="1">10</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Unknown</td>
<td rowspan="1" colspan="1">2</td>
<td rowspan="1" colspan="1">1.82</td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>Anatomic site</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">Tongue</td>
<td rowspan="1" colspan="1">68</td>
<td rowspan="1" colspan="1">61.82</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Lip</td>
<td rowspan="1" colspan="1">13</td>
<td rowspan="1" colspan="1">11.82</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Gingiva</td>
<td rowspan="1" colspan="1">7</td>
<td rowspan="1" colspan="1">6.36</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Cheek</td>
<td rowspan="1" colspan="1">5</td>
<td rowspan="1" colspan="1">4.55</td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>Maxillary sinus</bold>
</td>
<td rowspan="1" colspan="1">4</td>
<td rowspan="1" colspan="1">3.64</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Lower jaw</td>
<td rowspan="1" colspan="1">4</td>
<td rowspan="1" colspan="1">3.64</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Upper jaw</td>
<td rowspan="1" colspan="1">3</td>
<td rowspan="1" colspan="1">2.73</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Oral cavity</td>
<td rowspan="1" colspan="1">3</td>
<td rowspan="1" colspan="1">2.73</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Palate</td>
<td rowspan="1" colspan="1">1</td>
<td rowspan="1" colspan="1">0.91</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Parotid gland</td>
<td rowspan="1" colspan="1">1</td>
<td rowspan="1" colspan="1">0.91</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Mandible</td>
<td rowspan="1" colspan="1">1</td>
<td rowspan="1" colspan="1">0.91</td>
</tr>
</tbody>
</table>
</table-wrap>
<table-wrap id="T2" position="float">
<label>Table 2</label>
<caption>
<p>TAF1L protein expression in OSCC tissues or normal oral/paracancerous tissues by IHC</p>
</caption>
<table frame="hsides" rules="groups">
<thead valign="top">
<tr>
<th rowspan="1" colspan="1"></th>
<th rowspan="1" colspan="1">Case numbers (n)</th>
<th rowspan="1" colspan="1">Over-expression (n)</th>
<th rowspan="1" colspan="1">Over-expressive ratio (%)</th>
<th rowspan="1" colspan="1">
<italic>p</italic>
-value (Fisher's exact test)</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td rowspan="1" colspan="1">
<bold>Normal tissues</bold>
</td>
<td rowspan="1" colspan="1">30</td>
<td rowspan="1" colspan="1">9</td>
<td rowspan="1" colspan="1">28.1%</td>
<td rowspan="1" colspan="1">
<bold>0.0033*</bold>
</td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>OSCC tissues</bold>
</td>
<td rowspan="1" colspan="1">110</td>
<td rowspan="1" colspan="1">96</td>
<td rowspan="1" colspan="1">87.3%</td>
<td rowspan="1" colspan="1"></td>
</tr>
</tbody>
</table>
<table-wrap-foot>
<fn>
<p>* It means a statistically significant difference (
<italic>p</italic>
< 0.05).</p>
</fn>
</table-wrap-foot>
</table-wrap>
<table-wrap id="T3" position="float">
<label>Table 3</label>
<caption>
<p>The association between TAF1L protein overexpression and clinicopathological characteristics of OSCC patients</p>
</caption>
<table frame="hsides" rules="groups">
<thead valign="top">
<tr>
<th rowspan="2" colspan="1">Clinicopathological characteristics</th>
<th colspan="2" rowspan="1">TAF1L expression</th>
<th rowspan="1" colspan="1"></th>
</tr>
<tr>
<th rowspan="1" colspan="1">Low (n)</th>
<th rowspan="1" colspan="1">High (n)</th>
<th rowspan="1" colspan="1">
<italic>p</italic>
-value</th>
</tr>
</thead>
<tbody valign="top">
<tr>
<td rowspan="1" colspan="1">
<bold>Age (years)</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">≤50</td>
<td rowspan="1" colspan="1">13</td>
<td rowspan="1" colspan="1">44</td>
<td rowspan="1" colspan="1">0.6117</td>
</tr>
<tr>
<td rowspan="1" colspan="1">>50</td>
<td rowspan="1" colspan="1">10</td>
<td rowspan="1" colspan="1">43</td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>Gender</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">Female</td>
<td rowspan="1" colspan="1">2</td>
<td rowspan="1" colspan="1">40</td>
<td rowspan="1" colspan="1">0.7079</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Male</td>
<td rowspan="1" colspan="1">6</td>
<td rowspan="1" colspan="1">62</td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>Histological differentiation</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">Well</td>
<td rowspan="1" colspan="1">4</td>
<td rowspan="1" colspan="1">77</td>
<td rowspan="1" colspan="1">0.1654</td>
</tr>
<tr>
<td rowspan="1" colspan="1">Moderate, poor</td>
<td rowspan="1" colspan="1">3</td>
<td rowspan="1" colspan="1">19</td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>Clinical stage</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">I</td>
<td rowspan="1" colspan="1">8</td>
<td rowspan="1" colspan="1">4</td>
<td rowspan="1" colspan="1">0.2413</td>
</tr>
<tr>
<td rowspan="1" colspan="1">II-IV</td>
<td rowspan="1" colspan="1">51</td>
<td rowspan="1" colspan="1">27</td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">
<bold>T classification</bold>
</td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
<td rowspan="1" colspan="1"></td>
</tr>
<tr>
<td rowspan="1" colspan="1">T1</td>
<td rowspan="1" colspan="1">3</td>
<td rowspan="1" colspan="1">42</td>
<td rowspan="1" colspan="1">1</td>
</tr>
<tr>
<td rowspan="1" colspan="1">T2-4</td>
<td rowspan="1" colspan="1">57</td>
<td rowspan="1" colspan="1">58</td>
<td rowspan="1" colspan="1"></td>
</tr>
</tbody>
</table>
</table-wrap>
</floats-group>
</pmc>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
</list>
<tree>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Wang, Daiwei" sort="Wang, Daiwei" uniqKey="Wang D" first="Daiwei" last="Wang">Daiwei Wang</name>
</noRegion>
<name sortKey="Li, Ang" sort="Li, Ang" uniqKey="Li A" first="Ang" last="Li">Ang Li</name>
<name sortKey="Li, Yanpeng" sort="Li, Yanpeng" uniqKey="Li Y" first="Yanpeng" last="Li">Yanpeng Li</name>
<name sortKey="Liu, Qiong" sort="Liu, Qiong" uniqKey="Liu Q" first="Qiong" last="Liu">Qiong Liu</name>
<name sortKey="Liu, Qiong" sort="Liu, Qiong" uniqKey="Liu Q" first="Qiong" last="Liu">Qiong Liu</name>
<name sortKey="Qi, Hong" sort="Qi, Hong" uniqKey="Qi H" first="Hong" last="Qi">Hong Qi</name>
<name sortKey="Wang, Daiwei" sort="Wang, Daiwei" uniqKey="Wang D" first="Daiwei" last="Wang">Daiwei Wang</name>
<name sortKey="Wang, Yun" sort="Wang, Yun" uniqKey="Wang Y" first="Yun" last="Wang">Yun Wang</name>
<name sortKey="Zhang, Haoxing" sort="Zhang, Haoxing" uniqKey="Zhang H" first="Haoxing" last="Zhang">Haoxing Zhang</name>
<name sortKey="Zhou, Wei" sort="Zhou, Wei" uniqKey="Zhou W" first="Wei" last="Zhou">Wei Zhou</name>
</country>
</tree>
</affiliations>
</record>

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